Reproductive toxicology最新文献

{"title":"Maternal PM2.5 exposure causes fetal growth restriction and alters placental morphology: Role of uterine inflammation","authors":"Shan Wang,&nbsp;Hongxia Chen,&nbsp;Aryamann Singh,&nbsp;Niralkumar Ghevariya,&nbsp;Zhekang Ying","doi":"10.1016/j.reprotox.2026.109177","DOIUrl":"10.1016/j.reprotox.2026.109177","url":null,"abstract":"<div><div>Maternal exposure to fine particulate matter (PM_2.5) correlates with low birthweight. The mechanism, however, remains elusive. We thus investigated the effects of maternal PM_2.5 exposure on maternal uterus and placenta. To this end, female C57BL/6 J mice were exposed to filtered air (FA) or concentrated ambient PM_2.5 (CAP) for 20 weeks and then mated with normal males. Placentas and fetus of gestation day 18.5 were harvested and analyzed. Pregnancy outcomes were also assessed, and after weaning, the uteri of those subgroups of dams were collected and analyzed either at estrus or diestrus stage. Maternal CAP exposure significantly reduced the fetal and placental weights but not fetal-placental weight ratio. Histological analysis of placenta showed smaller junction zone and bigger decidua due to maternal CAP exposure, accompanied by uterine natural killer (uNK) cell infiltration in decidua but not remarkable changes in vasculature and mRNA expression of nutrient transporters. Moreover, CAP exposure reduced uterine mass and increased uterine macrophage infiltration at estrus, but not diestrus, stage. As such, we demonstrate that PM_2.5 exposure provokes endometritis, which may be responsible for the development of placental abnormalities and fetal growth restriction due to maternal PM_2.5 exposure, shedding light on the mechanism whereby maternal PM_2.5 exposure causes adverse reproductive outcomes.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109177"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent impact of in utero nanoparticle exposure on metabolic and endocrine outcomes in adult rats fed a high-fat diet","authors":"Russell Hunter,&nbsp;Teresa Gluth,&nbsp;Kate Seman,&nbsp;Travis Goldsmith,&nbsp;Riley Nett,&nbsp;Victoria Nist,&nbsp;Allison Dunn,&nbsp;Eric Kelly,&nbsp;Elizabeth Bowdridge","doi":"10.1016/j.reprotox.2025.109140","DOIUrl":"10.1016/j.reprotox.2025.109140","url":null,"abstract":"<div><div>Gestational nano titanium-dioxide (nano-TiO₂) exposure causes reduced fetal size and multi-generational reproductive effects in females. The current study utilized a whole-body nano-TiO₂ inhalation exposure model in pregnant Sprague-Dawley rats coupled with a high fat diet (HFD) fed to adult offspring to examine lasting effects of <em>in-utero</em> exposures on weight gain, metabolic function, and endocrine perturbations. Sexually dimorphic responses in weight gain were observed whereby exposed HFD males gained less weight than their air HFD counterparts (435 g ± 9.8 vs. 505 g ± 14.5; p &lt; 0.05), but there was no weight difference between air and exposed HFD females. Males and females presented with exposure driven decreases in glucose tolerance, such that HFD exposed animals were significantly more glucose intolerant(-6985AUC±1763). Hypothalamic gene expression of the melanocortin receptor 3 was significantly increased in nano-TiO₂ males (1453 %) and significantly decreased in nano-TiO₂ females (29.07 %) compared to grain-based diet (GBD) controls. Hepatic mitochondrial activity was affected in sexually dependent manner, with females exhibiting changes in Complexes I, II, III, and V, and males only showing differences in Complex I activity. Finally, exposed males had smaller testicular mass (3.685 mg ± 0.0895 in GBD; 3.358 mg±0.0786 in HFD; (3.480 mg± 0.2023 in GBD, 3.380 mg± 0.0777) and reduced testosterone (7.75 µg/nl ± 1.965 in GBD; 3.62 µg/nl±2.084 in HFD; (9.943 µg/nl±1.97 in GBD, 4.28 µg/nl± 1.6845) compared to air males. Altogether, these data reflect how nanoparticulate driven differences in growth and development at birth can alter weight gain and metabolic function later in life in the face of a dietary challenge.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109140"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Total flavonoids of Epimedium ameliorate testicular damage via keap1–Nrf2/ARE signalling and multi-target regulation","authors":"Hongchao Yuan ,&nbsp;Wenhao Tian ,&nbsp;Hao Hao ,&nbsp;Sirui Kang ,&nbsp;Fanfan Jia ,&nbsp;Kai Chen ,&nbsp;Xiaoying Zhang ,&nbsp;Chen Chen","doi":"10.1016/j.reprotox.2025.109142","DOIUrl":"10.1016/j.reprotox.2025.109142","url":null,"abstract":"<div><div>This study investigates the protective effects of total flavonoids of <em>Epimedium</em> (TFE) against obesity-induced testicular damage in mice. The potential pharmacological mechanisms were predicted using network pharmacology, molecular docking and molecular dynamics simulation. <em>In vivo</em> experiments were conducted in mice randomly assigned to five groups: a normal diet group, a high-fat diet (HFD) group, two TFE groups, and a positive control group. Biomarkers including dihydrotestosterone and testosterone were measured to evaluate testicular function, while lipid profiles were assessed. Oxidative stress was determined through glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) assays, and protein expression of heme oxygenase-1 (HO-1), NAD(P)H quinone dehydrogenase 1 (NQO1), nuclear factor erythroid 2-related factor 2 (Nrf2), and Kelch-like ECH-associated protein 1 (Keap1) was analysed. Network pharmacology identified 29 flavonoids and 288 key targets. Molecular docking revealed that 22 active components exhibited strong binding activity, with PLCZ1–isoginkgetin/bilobetin showing the most stable conformation. TFE treatment significantly improved testicular function and mitigated obesity-induced male infertility. It enhanced sperm quality, reversed HFD-induced reductions in sperm count and motility, decreased malformation rates, normalized serum testosterone and dihydrotestosterone levels, ameliorated oxidative stress by enhancing antioxidant enzyme activity (GSH) and reducing lipid peroxidation (MDA), and improved lipid profiles by lowering triglycerides (TG) while increasing high-density lipoprotein cholesterol (HDL-C). Mechanistically, TFE upregulated Nrf2 pathway components (HO-1, NQO1) and modulated Keap1 expression. Collectively, these findings establish that the protective effects of TFE against obesity-induced testicular damage are mediated by the coordinated regulation of oxidative stress and key testicular targets.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109142"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145782663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Male reproductive impairment linked to occupational ionizing radiation exposure in radiology workers","authors":"Tiinçe AKSAK ,&nbsp;Harika TOPAL ÖNAL ,&nbsp;İzzet OĞUZ","doi":"10.1016/j.reprotox.2026.109160","DOIUrl":"10.1016/j.reprotox.2026.109160","url":null,"abstract":"<div><div>Chronic occupational exposure to ionizing radiation (IR) may affect male reproductive health but the underlying genetic and immunologic mechanisms remain poorly defined. This study aimed to evaluate the effects of IR on semen quality, CD56-positive natural killer (NK) cell concentration and sperm nuclear protein gene expression. In this case-control study a total of 60 men were assessed 30 radiology workers with IR exposure and 30 men in the control group. Semen analysis was performed according to WHO 2021 criteria. NK cells were determined by CD56 immunocytochemical staining and mRNA expression levels of TNP1, TNP2 and CD56 were measured by qPCR. Compared with the control group the IR group had significantly lower sperm concentration and a higher frequency of morphological abnormalities (p &lt; 0.05). NK cell concentration was significantly increased (p &lt; 0.001) whereas TNP1 was significantly decreased (p &lt; 0.001). TNP1 mRNA levels were downregulated in exposed subjects whereas TNP2 expression showed a non-significant reduction. Weak to moderate correlations were observed between gene expression profiles and selected sperm parameters. In conclusion chronic occupational IR exposure is associated with impaired semen quality, heightened NK cell concentration and altered nuclear protein gene expression, potentially compromising male reproductive health. These findings highlight the need for reproductive health monitoring and protective strategies among radiation-exposed healthcare workers.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109160"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145906551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming and organelle quality control: The “silent” drivers of Sertoli cell dysfunction under environmental stressors","authors":"Meiying Feng ,&nbsp;Shuying Fu ,&nbsp;Kai Wang","doi":"10.1016/j.reprotox.2026.109173","DOIUrl":"10.1016/j.reprotox.2026.109173","url":null,"abstract":"<div><div>Sertoli cells (SCs) are the metabolic and structural “nurse” cells of the seminiferous epithelium. Classical testicular toxicology has largely focused on endpoints such as germ cell apoptosis, testicular atrophy and overt Sertoli cell death. These outcomes undoubtedly capture severe injury, but they are the last step in a longer pathogenic sequence. A growing body of work indicates that environmental toxicants and systemic metabolic stress reprogram SC energy metabolism and disrupt organelle quality control at sub-lethal levels long before cell death becomes evident. In this early phase, SCs lose their ability to sustain glycolysis–lactate shuttling, to recycle and oxidize lipids efficiently, and to maintain a healthy mitochondrial and lysosomal network, with important consequences for blood–testis barrier integrity and germ cell development. Here, we synthesize current evidence on SC-centered metabolic and organelle mechanisms in male reproductive toxicology. We first summarize the physiological roles of SCs in glycolysis and lactate export, lipid handling, mitochondrial dynamics, autophagy and LC3-associated phagocytosis, emphasizing how these pathways are coordinated to support spermatogenesis. We then discuss how selected environmental and systemic stressors—including atrazine, phthalates, cadmium, fine particulate matter (PM₂.₅), thermal stress and obesity—converge on these pathways to reprogram SC function. Building on these observations, we propose a two-phase model of SC injury in which sub-lethal metabolic and organelle misregulation represents an early, potentially reversible phase that precedes overt regulated cell death and structural collapse of the seminiferous epithelium. Finally, we highlight emerging therapeutic opportunities targeting SC metabolism and organelle quality control, and outline how incorporating SC-centered biomarkers into experimental designs could improve the sensitivity and mechanistic depth of reproductive risk assessment.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109173"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aqueous cigarette smoke extract reduces mitochondrial potential and increases nuclear degeneration in bovine oocytes matured in vitro","authors":"Ana Karen de Carvalho Albuquerque ,&nbsp;Solano Dantas Martins ,&nbsp;Leiz Maria Costa Véras ,&nbsp;Alyne Rodrigues de Araújo Nobre ,&nbsp;Vânia Marilande Ceccatto ,&nbsp;Valdevane Rocha Araújo","doi":"10.1016/j.reprotox.2025.109141","DOIUrl":"10.1016/j.reprotox.2025.109141","url":null,"abstract":"<div><div>This study investigated the cytotoxicity of different concentrations of aqueous extract of cigarette smoke (AECS) during in vitro maturation (IVM) of bovine oocytes, evaluating the potential synergy among its various compounds, including nicotine. The AECS was evaluated by liquid chromatography to identify nicotine amount and by atomic force microscopy (AFM) to analyze the morphology of particles. To IVM, bovine ovaries (n = 30) were collected in local slaughterhouse and submitted to slicing. Only oocytes that exhibited homogeneous cytoplasm, diameter higher than 110 µm, and surrounded by, at least, two layers of compact cumulus cells were selected. Cumulus-oocyte complex (COCs) were matured in groups under mineral oil in TCM-199 + alone (CTRL) or TCM-199 + supplemented with 1, 2.5 or 5 % of AECS, at 38,5°C in a humidified atmosphere containing 5 % CO2 in air for 24 h. After IVM period, oocytes were denuded and evaluated to chromatin configuration by Hoechst, and ROS and mitochondrial potential by H2DCFDA and JC-1, respectively. The data distribution was assessed using the Shapiro-Wilk test for homogeneity and ANOVA One-way with post hoc of Tukey considering P &lt; 0.05. The results revelated high nicotine levels (158.40 µg/mL) in the AECS and nanoparticles with 14,66 ± 4,08 nm of diameter. Regardless of AECS concentration used, high chromatin degenerated rates of oocytes after IVM, and an increase of ROS levels and a reduction of mitochondrial (P &lt; 0,05) was observed. Thus, it can be concluded that AECS exhibits significant cytotoxic properties towards bovine oocytes, particularly due to the presence of elevated concentrations of nicotine.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109141"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early gonadotoxic effects of cyclophosphamide on the prepubertal testis and the feasibility of reducing toxicity through combined antioxidant therapy","authors":"Amirhesam Eskafinoghani ,&nbsp;Arturo Reyes Palomares ,&nbsp;Xia Hao ,&nbsp;Roudabeh Mohammadi ,&nbsp;Arian Lundberg ,&nbsp;Kenny A. Rodriguez-Walberg","doi":"10.1016/j.reprotox.2025.109156","DOIUrl":"10.1016/j.reprotox.2025.109156","url":null,"abstract":"<div><div>Early chemotherapy-induced gonad toxicity threatens future fertility in boys, yet early in-vivo testicular responses are poorly defined. To characterize acute effects of cyclophosphamide (CPA) on the prepubertal testis and explore whether combined antioxidants (AO; <span>L</span>-carnitine [LC] and N-acetyl cysteine [NAC]) modulate these changes. CBA/B6 F1 male pups (postnatal day 7–9) were randomized to saline control, CPA (100 mg/kg i.p.), AO, or CPA+AO. Testes were collected every 8 h to 48 h for histology/immunostaining and were pooled (n = 3 per group/time point) for bulk RNA-seq per group/time point. Histology showed emerging degeneration from ∼32 h with prominent effects by 48 h after CPA, including reduced germ cell layers, increased γH2AX/CC3, and decreased Ki67. Transcriptionally, CPA perturbed apoptosis/developmental pathways as early as 16 h, preceding overt histological change. AO and CPA+AO groups displayed partial transcriptional shifts toward control profiles, consistent with mitigation of CPA-associated signatures, but not full normalization. In neonatal mouse testis, CPA elicits rapid transcriptomic reprogramming within 16 h, before morphological injury at ∼32–48 h. Concomitant AO shows preliminary, partial protective transcriptional effects. These proof-of-concept data support transcriptomics as an early, sensitive readout of testicular toxicity and motivate follow-up studies with independent validation and long-term outcomes prior to clinical translation.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109156"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uptake of polystyrene nanoplastics by cumulus-oocyte complexes impairs oocyte and embryo development","authors":"Jiayi Yang ,&nbsp;Kaylee Nieuwland ,&nbsp;Nikita L. Korpel ,&nbsp;Richard W. Wubbolts ,&nbsp;Juliette Legler ,&nbsp;Jorke H. Kamstra ,&nbsp;Hilde Aardema","doi":"10.1016/j.reprotox.2026.109181","DOIUrl":"10.1016/j.reprotox.2026.109181","url":null,"abstract":"<div><div>Nanoplastics (NPs), plastic particles smaller than 1 μm, have gained increasing attention due to their potential health effects. Experimental studies in animals have shown that NPs can pass biological barriers, reach the female reproductive tract, and enter the ovary. Their presence in the ovary might have profound consequences for reproductive endpoints, such as oocyte development. This study aimed to investigate the uptake and associated effects of polystyrene (PS) NPs on oocyte and embryo development using a bovine <em>in vitro</em> fertilization (IVF) model. Bovine cumulus-oocyte complexes (COCs) were exposed to pristine PS-NPs (50 nm or 200 nm) at different doses during <em>in vitro</em> maturation (23 h), followed by IVF and embryo culture. RNA sequencing was performed to investigate mechanisms involved in possible effects on oocyte maturation. Confocal microscopy confirmed the internalization of 50 nm and 200 nm PS-NPs into cumulus cells, however, only 50 nm particles were able to transfer into oocytes. Additionally, exposure to 50 nm PS-NPs at 3 μg/mL significantly delayed oocyte nuclear maturation and early embryo development. At this dose, RNA sequencing did not identify differentially expressed genes in the COCs, however, gene set enrichment analyses did indicate effects on mitochondrial processes. Nevertheless, subsequent analysis on mitochondrial activity remained unaffected. Our findings suggest that while 50 nm PS-NPs can penetrate the zona pellucida and impair oocyte maturation, their effects may not be driven by major transcriptomic or mitochondrial functional alterations.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109181"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146132779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypothesis-driven approach to developmental toxicity assessment: Using mechanistic information to inform testing","authors":"George Daston ,&nbsp;Matthew Burbank ,&nbsp;Florian Gautier ,&nbsp;Barbara F. Hales ,&nbsp;Amer Jamalpoor ,&nbsp;Yasunari Kanda ,&nbsp;Susan Makris ,&nbsp;Aldert H. Piersma ,&nbsp;Nicola Powles-Glover ,&nbsp;Sonya Sobrian ,&nbsp;Vicki Sutherland ,&nbsp;Steven Van Cruchten ,&nbsp;Ronald L. Wange ,&nbsp;Connie L. Chen","doi":"10.1016/j.reprotox.2025.109119","DOIUrl":"10.1016/j.reprotox.2025.109119","url":null,"abstract":"<div><div>Developmental toxicity assessment relies on standardized guideline protocols in which animals (usually rats and/or rabbits) are exposed to the test(s) agent(s) and pregnancy outcomes are assessed at an organismal level. Increasing information about mechanisms of toxicity now allows improved selection of in vivo and in vitro models for assessing developmental toxicity and prediction of developmental outcome by investigating the mode of action (MoA) of the test agent, allowing for a more flexible resource-efficient approach. Read-across, already widely used for chemical assessment, relies on a combination of cheminformatics to select suitable analogs and any of a variety of methods to prove biological similarity and/or a common metabolic pathway. Some of these methods include high-throughput test batteries (e.g., ToxCast) and transcriptomics linked to large databases of gene expression profiles. These can be used to both generate and test hypotheses about MoA of novel compounds. Increasing availability of induced pluripotent stem cells provides greater range of biological models that closely mimic the human biology relevant for addressing a specific hypothesis. Examples are given of how (1) understanding mode of action can be used to identify activity cliffs in a series of analogous chemicals, (2) the use of metabolism data in an example demonstrating that closely related analogs do not all have to be tested in developmental toxicity protocols, and (3) how analysis of gene expression can be used to identify divergent pharmacology in similar chemicals. It is possible using the approaches described to design more flexible, hypothesis-driven approaches to assess developmental toxicity.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109119"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145655315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urban air pollution and in vitro fertilization outcomes: A Canadian retrospective study","authors":"Vasilia Vastis ,&nbsp;Riki Dayan ,&nbsp;Michael Neal ,&nbsp;Stacy Deniz ,&nbsp;Shilpa Amin ,&nbsp;Megan Karnis ,&nbsp;Karen Kteily ,&nbsp;Catherine Friedman ,&nbsp;Alison Holloway ,&nbsp;Kerstyn Lutz ,&nbsp;João Réquia Júnior Weeberb ,&nbsp;Matthew Adams ,&nbsp;Mehrnoosh Faghih","doi":"10.1016/j.reprotox.2026.109161","DOIUrl":"10.1016/j.reprotox.2026.109161","url":null,"abstract":"<div><div>There is growing data to support an adverse relationship between air pollution and fertility. Many studies have shown that traffic-related air pollution, the most common source of urban air pollution in North America, has a negative effect on both spontaneous and IVF pregnancy outcomes. This single-center retrospective study is the first Canadian study to explore urban air pollution exposures and IVF/ICSI outcomes. It included autologous IVF/ICSI outcomes from both fresh (ET – n = 1756) and frozen embryo transfer (FET – n = 1535) cycles between 2000 and 2022. Air pollution data for fine particulate matter (PM2.5) and nitrogen dioxide (NO₂) were obtained from The Canadian Urban Environmental Health Research Consortium (CANUE). Data was analyzed using bivariate maps of long-term air pollutant exposure (PM2.5 and NO₂) and IVF/ICSI clinical outcomes by 5 km² urban areas. We found that long-term air pollution within patients’ household area ranged from 4.8 to 12.6 μg/m³ for PM2.5 and 3.2–28 ppb for NO₂. Nitrogen dioxide has demonstrated an association to some IVF/ICSI outcomes, which agrees with other international studies. No statistical associations in IVF/ICSI outcomes were found after adjusting for confounding variables. Understanding of the impact of urban air pollution on fertility and IVF/ICSI outcomes warrants further research on interventions to ameliorate negative outcomes and supports policy change(s) to improve air quality in the future.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109161"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145945751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}