Reproductive toxicology最新文献

{"title":"Analyzing high-throughput assay data to advance the rapid screening of environmental chemicals for human reproductive toxicity.","authors":"Julia R Varshavsky, Juleen Lam, Courtney Cooper, Patrick Allard, Jennifer Fung, Ashwini Oke, Ravinder Kumar, Joshua F Robinson, Tracey J Woodruff","doi":"10.1016/j.reprotox.2024.108725","DOIUrl":"10.1016/j.reprotox.2024.108725","url":null,"abstract":"<p><p>While high-throughput (HTP) assays have been proposed as platforms to rapidly assess reproductive toxicity, there is currently a lack of established assays that specifically address germline development/function and fertility. We assessed the applicability domains of yeast (S. cerevisiae) and nematode (C. elegans) HTP assays in toxicity screening of 124 environmental chemicals, determining their agreement in identifying toxicants and their concordance with reproductive toxicity in vivo. We integrated data generated in the two models and compared results using a streamlined, semi-automated benchmark dose (BMD) modeling approach. We then extracted and modeled relevant mammalian in vivo data available for the matching chemicals included in the Toxicological Reference Database (ToxRefDB). We ranked potencies of common compounds using the BMD and evaluated correlation between the datasets using Pearson and Spearman correlation coefficients. We found moderate to good correlation across the three data sets, with r = 0.48 (95 % CI: 0.28-1.00, p<0.001) and r_s = 0.40 (p=0.002) for the parametric and rank order correlations between the HTP BMDs; r = 0.95 (95 % CI: 0.76-1.00, p=0.0005) and r_s = 0.89 (p=0.006) between the yeast assay and ToxRefDB BMDs; and r = 0.81 (95 % CI: 0.28-1.00, p=0.014) and r_s = 0.75 (p=0.033) between the worm assay and ToxRefDB BMDs. Our findings underscore the potential of these HTP assays to identify environmental chemicals that exhibit reproductive toxicity. Integrating these HTP datasets into mammalian in vivo prediction models using machine learning methods could further enhance their predictive value in future rapid screening efforts.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108725"},"PeriodicalIF":3.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142473602","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":"Mixed exposure to PFOA and PFOS induces oocyte apoptosis and subfertility in mice by activating the Hippo signaling pathway.","authors":"Xiang-Zhu Yan, Jia Peng, Yu-Qing Liu, Ruo-Nan Fan, Xin-Yi Ni, Ling Gong, Dan-Ni Zhang, Xin Huang, Shu-Hua Tan, Hai-Long Wang","doi":"10.1016/j.reprotox.2024.108829","DOIUrl":"https://doi.org/10.1016/j.reprotox.2024.108829","url":null,"abstract":"<p><p>Per- and polyfluoroalkyl substances (PFAS) are synthetic perfluorinated compounds known for their persistence in the environment and reproduction toxicity. PFAS, perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS), have been identified in the follicular fluid of infertile women. However, the specific of PFOA and PFOS mixture on oocyte quality and female fertility remain unclear. In this study, we exposed female mice to combination of PFOA and PFOS to investigate the underlying mechanisms impairing fertility and oocyte maturation. Our results showed that exposure to the mixture induced epigenetic alterations and DNA damage in oocytes, impairing meiosis. Additionally, mitochondrial dysfunction caused by the exposure to the mixture led to oxidative stress and apoptosis in the oocytes. The reduction in oocyte quality resulted in a decrease in blastocyst quality and litter size. Furthermore, single-cell transcriptome analysis indicated that exposure to the mixture disrupted energy metabolism and triggered apoptosis, possibly through the activation of the Hippo signaling pathway. Overall, our results suggest that exposure to PFOA and PFOS mixture impairs the fertility in mice through the activation of the Hippo signaling pathway-induced oocytes apoptosis.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108829"},"PeriodicalIF":3.3,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922789","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":"Perfluoroalkyl substances (PFAS) exposure and preeclampsia risk: Impaired angiogenesis through suppression of VEGF signaling.","authors":"Jay S Mishra, Bradley Bosse, Kara K Hoppe, Kristen Malecki, Scott J Hetzel, Sathish Kumar","doi":"10.1016/j.reprotox.2024.108827","DOIUrl":"10.1016/j.reprotox.2024.108827","url":null,"abstract":"<p><p>Per- and polyfluoroalkyl substances (PFAS) are linked to preeclampsia (PE), a condition involving abnormal angiogenesis. Prior research on this association has been inconclusive. We investigated the relationship between maternal PFAS exposure and PE risk in Wisconsin. We also examined if PFAS disrupts angiogenesis and, if so, what mechanisms are involved. We conducted a case-control study with 40 PE cases and 40 controls. Maternal serum was analyzed for 38 different PFAS compounds using LC MS/MS. Functional in vitro experiments assessed PFOS effects on angiogenesis and mechanisms. Maternal serum samples from women with PE exhibited significantly higher PFOS and PFHPS concentrations than controls. After adjusting for confounders, each log-scale IQR increase in PFOS and PFHPS concentrations was associated with a 7.18-fold (95 % CI: 2.24, 23.0) and 5.40-fold (95 % CI: 1.81, 16.1) higher odds of PE, respectively. Furthermore, PFOS and PFHPS were positively associated with sFLT1 levels and the sFLT1/PLGF ratio. In vitro experiments revealed that PFOS exposure impaired HUVEC proliferation, migration, and tube formation, essential processes for angiogenesis. The membrane-based antibody array showed that PFOS decreased expression of multiple angiogenic proteins, including I-TAC, uPAR, VEGFR2, MMP-1, IL-1α, Angiopoietin-2, IL-1β, PECAM-1, TIE-2, and TIMP-2. The qPCR analysis demonstrated that PFOS decreased VEGFR2, the upstream target of VEGF, at the transcriptional level. In conclusion, elevated PFAS, especially PFOS and PFHPS, are linked to increased PE risk. PFOS may suppress angiogenesis via attenuated VEGFR2-mediated signaling, providing a molecular mechanism linking PFAS and PE pathogenesis.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108827"},"PeriodicalIF":3.3,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896576","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":"Computational insights into maternal environmental pollutants and folate pathway regulation.","authors":"Adarsh Kumar Shukla, Shadab Ahamad, Prachi Kukshal","doi":"10.1016/j.reprotox.2024.108825","DOIUrl":"https://doi.org/10.1016/j.reprotox.2024.108825","url":null,"abstract":"<p><p>Exposure to environmental pollutants during pregnancy can adversely affect fetal growth and postnatal development. While numerous studies have explored the interaction between environmental toxic chemicals and the folate pathway, few have examined their inhibitory effects on key targets. This computational study identified 27 maternal environmental toxicants using the Comparative Toxicogenomics Database (CTD) and analyzed them to identify their targets. Molecular modeling, docking, and dynamics simulations revealed that folate receptors (FOLR1, FOLR2, and FOLR3) and transporters (SLC19A1 and SLC46) are major targets. Among these, FOLR3 exhibited the strongest interactions with toxicants such as Dichlorodiphenyltrichloroethane (DDT), Bisphenols, Dioxin, and other investigated toxicants. Toxicity profiling showed that even minimal exposure to these pollutants significantly impacts maternal health and disrupts folate metabolism, leading to fetal malformations. This study highlights the critical role of maternal toxicants in hindering the folate pathway, with severe implications for fetal development.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108825"},"PeriodicalIF":3.3,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142897282","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":"Alogliptin attenuates testicular damage induced by monosodium glutamate in both juvenile and adult male rats by activating autophagy: ROS Dependent AMPK/mTOR.","authors":"Manal Mohammad Morsy, Heba A Hassan, Reham M Morsi, Ola Elsayed Nafea, Azza I Farag, Rania Saad Ramadan","doi":"10.1016/j.reprotox.2024.108826","DOIUrl":"https://doi.org/10.1016/j.reprotox.2024.108826","url":null,"abstract":"<p><p>Monosodium glutamate (MSG) is one of the most commonly used food additives, known for its adverse health effects. Alogliptin (ALO) is a highly selective dipeptidyl peptidase-4 inhibitor, but its role in male reproductive function remains debated. The study was designed to evaluate and compare the potential of ALO in mitigating MSG-induced testicular toxicity in juvenile and adult male rats. Juvenile and adult male rats were treated with either MSG or pretreated with ALO before MSG administration. Subsequently, rats concurrently received ALO plus MSG concurrently for 28 days. Testicular tissues were isolated and subjected to histo-biochemical and molecular assessments. Our results demonstrated that ALO reversed MSG-induced testicular injury, as evidenced by the restoration of reproductive hormone balance (increased serum luteinizing hormone and testosterone concentrations), suppression of oxidative stress injury (decreased testicular malondialdehyde, increased superoxide dismutase activity, and minimal 8-hydroxy-2'-deoxyguanosine immunoreactivity), inflammation (reduced testicular tumor necrosis factor-alpha levels), and fibrosis (decreased testicular collagen fiber deposition). Additionally, ALO impeded apoptosis and activated autophagy by decreasing caspase-3 activity, stimulating the AMPK/mTOR pathway, downregulating Bax and SQSTM-1/p62 expression, upregulating Bcl2 and Beclin 1, promoting testicular proliferation (increased number of proliferating cell nuclear antigen-positive cells in the testis), restoring glycogen content in the testis (mild to moderate periodic acid-Schiff reaction), and preserving testicular architecture. MSG induced more severe adverse testicular effects in juvenile rats, while ALO pretreatment was more protective in adult rats. ALO's anti-inflammatory, antioxidant, antiapoptotic, pro-autophagic, antifibrotic, and proliferative actions in the testis suggest its promising potential for combating male reproductive dysfunction.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108826"},"PeriodicalIF":3.3,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142897280","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":"Role of the endocannabinoid system in gonadal development: Implications for endocrine disruption and reproductive toxicity.","authors":"Anderson Tadeu de Araújo-Ramos, Anderson Joel Martino-Andrade","doi":"10.1016/j.reprotox.2024.108822","DOIUrl":"10.1016/j.reprotox.2024.108822","url":null,"abstract":"<p><p>The endocannabinoid system (ECS) plays a pivotal role in reproductive physiology, including gonadal development, though its influence on testis and ovary development has only recently gained attention. The ECS comprises lipid-derived ligands such as anandamide (AEA) and 2-arachidonoylglycerol (2-AG), along with cannabinoid receptors CB1 and CB2, which are expressed in various gonadal cells. Emerging research indicates that ECS signaling is critical for testosterone synthesis and gonadal cell proliferation and differentiation. This review explores the expression and function of ECS components in developing gonads, highlighting the differential roles of CB1 and CB2 receptors in species-specific contexts. Furthermore, the ECS has been suggested to be involved in the adverse effects of endocrine-disrupting chemicals (EDCs) on reproductive development. EDCs, such as phthalates, may interfere with ECS signaling, potentially leading to reproductive abnormalities that resemble the human Testicular Dysgenesis Syndrome (TDS). Understanding the molecular interactions between EDCs and the ECS could reveal novel mechanisms underlying reproductive toxicities. Future research should focus on the detailed localization and temporal expression of ECS components in fetal gonads, the mechanisms of cannabinoid-mediated testosterone inhibition, and the potential direct interaction of EDCs with the ECS. This knowledge could be crucial for developing strategies to mitigate reproductive health risks associated with EDC exposure.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108822"},"PeriodicalIF":3.3,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142872591","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":"Evaluation of the effect of rozanolixizumab on pregnancy outcomes and pre- and postnatal development in cynomolgus monkeys.","authors":"Annick Cauvin, Kevin Brady, Joy Cavagnaro, C Marc Luetjens","doi":"10.1016/j.reprotox.2024.108823","DOIUrl":"https://doi.org/10.1016/j.reprotox.2024.108823","url":null,"abstract":"<p><p>Rozanolixizumab, a humanised immunoglobulin (Ig) G4 monoclonal antibody that selectively inhibits binding of IgG to the neonatal Fc receptor (FcRn), was evaluated in an embryo-foetal enhanced pre- and postnatal development (ePPND) study. Pregnant female cynomolgus monkeys (19 per group) received subcutaneous rozanolixizumab 50mg/kg or 150mg/kg or vehicle every 3 days from gestation day 20 until delivery. The proportion of pregnancy losses was 15.8%, 21.1% and 5.3%, in the rozanolixizumab 50mg/kg, 150mg/kg and control groups, respectively. Based on eNormograms for groups of 18 or 20 animals, these results were considered to be within the range of spontaneous prenatal losses naturally observed in cynomolgus monkeys. Foetal examinations revealed no treatment-related effects. All infants had normal postnatal development, although higher mortality was observed in female infants from the control group during the first 3 weeks. All infants were able to mount a normal immune response to keyhole limpet haemocyanin when vaccinated at the age of 4 months. Offspring from 150mg/kg-treated mothers had very low IgG levels at birth, indicating blockade of maternal IgG transfer; infants from mothers who received 50mg/kg had variable IgG levels at birth, with mothers who had developed significant anti-drug antibodies conferring maternal IgG transfer to varying degrees. Rates of infection in infants were similar across treatment groups. IgG levels in infants from rozanolixizumab-treated groups normalised within 2 months. Treatment of pregnant cynomolgus monkeys with the FcRn inhibitor rozanolixizumab had no adverse effects on pre- or postnatal development of offspring, including immune system development.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108823"},"PeriodicalIF":3.3,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142872588","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":"Embryotoxicity of statins and other prescribed drugs with reported off-target effects on cholesterol biosynthesis.","authors":"Taryn Hartley, Hagir Abdelmagid, Zeenat Abdulsalam, Aliyah Mansion, Emily Howe, Daniel Ramirez, Kaylei White, Emmanuel Tadjuidje","doi":"10.1016/j.reprotox.2024.108820","DOIUrl":"10.1016/j.reprotox.2024.108820","url":null,"abstract":"<p><p>Cholesterol plays pivotal cellular functions ranging from maintaining membrane fluidity to regulating cell-cell signaling. High cholesterol causes cardiovascular diseases, low cholesterol is linked to neuropsychiatric disorders, and inborn errors of cholesterol synthesis cause multisystem malformation syndromes. Statins lower cholesterol levels by inhibiting the first, rate-limiting reaction of the cholesterol biosynthesis pathway catalyzed by hydroxymethyl-glutaryl-Coenzyme A reductase (HMGCR). However, they have also been shown to interfere with cellular pathways that are unrelated to cholesterol synthesis. One of the last enzymes of cholesterol biosynthesis, 7-dehydrocholesterol reductase (DHCR7), is often mutated in the Smith-Lemli-Opitz syndrome (SLOS), a multisystem malformation syndrome. Strikingly, recent studies have shown that some prescribed psychotropic pharmaceuticals inhibit its activity. In this study, we used Xenopus laevis as a model organism to test the effects of 8 FDA-approved statins and selected prescribed psychotropic drugs on the developing vertebrate embryo. Drugs were tested at concentrations ranging from 0.1 µM to 50 µM. Embryos were exposed to the drugs from the blastula stage through the swimming tadpole stage with daily medium change. Our data show that statins are heterogenous with respect to their ability to cause embryonic lethality, with simvastatin, pitavastatin, lovastatin, cerivastatin, and fluvastatin being the most toxic ones. Observed phenotypes included delayed development, shortened body axis and pericardiac edema. On the other hand, psychotropic drugs were less embryonic lethal than statins but caused similar phenotypes as well as microcephaly and holoprosencephaly. Our findings suggest that the proximal and distal inhibition of cholesterol biosynthesis have different but overlapping effects on embryonic development.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108820"},"PeriodicalIF":3.3,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819088","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":"Quaternary ammonium compound exposure causes infertility by altering endocrine signaling and gametogenesis.","authors":"Zachary A Kirkpatrick, Vanessa E Melin, Terry C Hrubec","doi":"10.1016/j.reprotox.2024.108817","DOIUrl":"10.1016/j.reprotox.2024.108817","url":null,"abstract":"<p><p>Quaternary ammonium compounds (QACs) are common substances utilized in cleaners, ophthalmic solutions, swimming pool treatments, cosmetics, and other consumer goods. Previous studies have shown that QAC exposure causes infertility in both male and female mice. Based on these studies, we hypothesized that oral QAC exposure negatively impacts male and female reproduction through changes in physiologic and endocrine mechanisms rather than direct toxicity to gametes. Endocrine disruption was assessed by evaluating luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations in male and female mice exposed orally throughout gestation and lactation, and by changes in estrogen and progesterone in in orally exposed females throughout pregnancy. Sperm functionality and spermatogenesis were assessed by in vitro fertilization; while Sertoli cell homeostasis was evaluated by determining cellular metabolism, cell cycle progression and blood-testes barrier (BTB) permeability. QAC exposure decreased LH, and FSH concentrations in both males and females, and decreased progesterone and estrogen concentrations during pregnancy. QACs significantly decreased Sertoli cell metabolism at 0.0005 % ADBAC+DDAC well before disruption of the BTB at 0.01 %. Fertilization was not affected 24 h after exposure but was decreased after a 10 day rest period suggesting a disruption in spermatogenesis rather than direct toxicity to sperm. Lastly, QAC exposure altered Sertoli cell cycling with a G2/M cycle arrest. While the effect of QAC exposure on humans is unknown, implications from the in vivo and in vitro studies are concerning given the rise in infertility rates and increased reliance on assisted reproductive technologies along with ubiquitous exposure to QACs.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108817"},"PeriodicalIF":3.3,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801573","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":"Maternal exposure to fine particulate matter in the air and risk for fetal congenital heart defects: a case-control study.","authors":"Zhao Li, Di Wang, Lei Jin, Jie Zhang, Tao Xue, Lei Jin","doi":"10.1016/j.reprotox.2024.108816","DOIUrl":"https://doi.org/10.1016/j.reprotox.2024.108816","url":null,"abstract":"<p><p>Prior research into the association between fine particulate matter (PM_2.5) exposure and the risk for fetal congenital heart defect (CHD) has yielded inconclusive and conflicting results. More epidemiologic evidence from different regions is necessary. A case-control study was conducted with 360 CHD cases and 3600 healthy newborns. Both the cases and the controls were registered by the mothers in the Prenatal Health Care System during the first trimester and gave birth at hospitals in the Tongzhou District of Beijing between 2013 and 2018. Information on PM_2.5 was obtained from satellite remote sensing monitoring data. We estimated average monthly PM_2.5 exposure for participants from 3 months before the last menstrual period through 6 months of gestational period. A logistic regression model was used to estimate odd ratio (OR) (95% confidence interval, CI) for PM_2.5 exposure level and fetal risk for CHD. In our study, PM_2.5 concentrations before pregnancy and in the first trimester were not associated with CHD risk. In the second trimester, 2^nd high quartile PM_2.5 group during the second month were associated with a lower CHD risk (adjusted OR(aOR)=1.42, 95% CI: 1.04-1.94) and highest quartile level group of PM_2.5 exposure in the third month were associated with a reduced risk for fetal CHD (aOR=0.70, 95% CI: 0.51-0.97). After Bonferroni's α correction, no comparisons were statistically significant. In conclusion, no associations were found between PM_2.5 exposure level and fetal risk for CHD in our study.</p>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":" ","pages":"108816"},"PeriodicalIF":3.3,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142787025","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}