Reproductive toxicology最新文献_第3页

Intestinal microbiome in response to air pollutant exposure in pregestational and gestational murine females and their male and female offspring 妊娠期和妊娠期雌性小鼠及其雌雄后代肠道微生物组对空气污染物暴露的响应。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-23 DOI: 10.1016/j.reprotox.2025.109150

Shubhamoy Ghosh , Amit Ganguly , Tien S. Dong , Venu Lagishetty , Jonathan P. Jacobs , Sherin U. Devaskar

{"title":"Intestinal microbiome in response to air pollutant exposure in pregestational and gestational murine females and their male and female offspring","authors":"Shubhamoy Ghosh , Amit Ganguly , Tien S. Dong , Venu Lagishetty , Jonathan P. Jacobs , Sherin U. Devaskar","doi":"10.1016/j.reprotox.2025.109150","DOIUrl":"10.1016/j.reprotox.2025.109150","url":null,"abstract":"<div><div>We investigated the impact of chronic air pollutant (AP) exposure upon intestinal microbial diversity, composition, and metagenomic inferred functional pathways in murine pregestational and late gestational adult females, and male and female postnatal offspring (P21), compared to age- and sex- matched controls (CON). Intestinal microbiome analysis was undertaken with certain phenotypic characteristics in adult non-pregnant and pregnant females and the male and female offspring. In response to AP, pooled male and female offspring displayed no difference in E19 fetal and P1 postnatal body weights. At P21, females exposed in-utero to AP were heavier with increased fat and muscle mass at one month versus CON. Males were no different at P21 and 1 month revealing decreased fat mass and hyperglycemia. In pregestational/gestational females, AP did not change microbial α- or β-diversity from the respective CON. Gestational females showed AP induced changes in taxonomic composition such as reduced Bacteroides and increased Firmicutes, Verrucomicrobia, and Akkermansia, among others. In response to intra-uterine AP exposure, the offspring intestinal microbiome revealed more compelling differences in α- and β- diversity than adult females. While certain microbial changes were common in both sexes, sex-specific differences also emerged with reduced α-diversity, decreased Bacteroides and increased Akkermansia in males only. The metagenomic inferred pathways revealed perturbations in multiple pathways. We conclude that the offspring exposed in-utero to AP revealed sex-specific changes in microbial diversity, composition and function, displaying certain similarities with distinct differences from mothers. These early life changes were associated with the subsequent emergence of pre-diabetes and adiposity.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109150"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145834609","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}

引用次数: 0

Corrigendum to “Irreversible male infertility from sleep restriction: A dual hit on testicular steroidogenesis and Keap1-Nrf2-mediated antioxidant defense” [Reprod. Toxicol. 138 (2025), 109083] “睡眠不足导致的不可逆转的男性不育：睾丸甾体激素生成和keap1 - nrf2介导的抗氧化防御的双重打击”的更正。中国生物医学工程学报，2003,19(5):393 - 393。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-08 DOI: 10.1016/j.reprotox.2025.109135

Keke Chen , Fengyou Luo , Xiling Huang , Kaixing Huang , Xiaoyu Liu , Qiping Hu , Changlong Xu

引用次数: 0

Perfluorodecanoic acid (PFDA) induces oxidative stress and autophagy dysregulation in HGrC1 cells 全氟癸酸（PFDA）诱导HGrC1细胞氧化应激和自噬失调。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-09 DOI: 10.1016/j.reprotox.2025.109136

Rasha A. Barakat , Changyong Lee , Hannah B. Ball , Kendra L. Clark

{"title":"Perfluorodecanoic acid (PFDA) induces oxidative stress and autophagy dysregulation in HGrC1 cells","authors":"Rasha A. Barakat , Changyong Lee , Hannah B. Ball , Kendra L. Clark","doi":"10.1016/j.reprotox.2025.109136","DOIUrl":"10.1016/j.reprotox.2025.109136","url":null,"abstract":"<div><div>Perfluorodecanoic acid (PFDA), a long-chain per- and polyfluoroalkyl substance (PFAS), is an emerging environmental toxicant, though little is known on its impact on female reproduction. This study investigates the cellular effects of PFDA on a human granulosa cell line, HGrC1, focusing on oxidative stress and autophagy pathways. HGrC1 cells were exposed to increasing concentrations (0.01 – 10 µM) of PFDA for 24, 48, 72, and 96 h. Notably, 10 µM PFDA for 48 h resulted in approximately 50 % reduction in cell viability, activation of cleaved caspase-3, reduced cell density, and altered morphology characterized by spindle-shaped elongation. qRT-PCR revealed significant downregulation of key antioxidant genes, particularly catalase. PFDA exposure markedly increased intracellular reactive oxygen species levels. Western blot analysis of the p62-Keap1-Nrf2 signaling pathway showed decreased KEAP1 protein levels and strong nuclear accumulation of NRF2 at 10 µM PFDA, supported by elevated expression of the downstream target HO-1. In parallel, PFDA disrupted autophagy regulation. Accumulation of p62, along with increased levels of LC3A/B, suggested impaired autophagic flux. Together, these findings demonstrate that PFDA compromises granulosa cell survival by inducing oxidative stress, altering antioxidant gene expression, and dysregulating autophagy. Given the central role of granulosa cells in follicular development and hormone synthesis, PFDA-induced toxicity may have significant implications for ovarian function and female fertility.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109136"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145744278","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}

引用次数: 0

Clonidine compromises human sperm functions 可乐定会损害人类精子功能

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2026-01-08 DOI: 10.1016/j.reprotox.2026.109164

Xuchang Liu , Yanfan Cui , Ruirui Qian , Yixuan Li , Zeyu Hu , Houyang Chen , Yufeng Yuan , Tao Luo

{"title":"Clonidine compromises human sperm functions","authors":"Xuchang Liu , Yanfan Cui , Ruirui Qian , Yixuan Li , Zeyu Hu , Houyang Chen , Yufeng Yuan , Tao Luo","doi":"10.1016/j.reprotox.2026.109164","DOIUrl":"10.1016/j.reprotox.2026.109164","url":null,"abstract":"<div><div>Although clonidine, a widely prescribed α2-adrenergic agonist for hypertension and attention deficit hyperactivity disorder (ADHD), has unknown effects on male fertility. This study investigated clonidine's impact on human sperm function and progesterone-induced signaling pathways essential for fertilization. To address this knowledge gap, human sperm from normozoospermic donors (n ≥ 4 per experiment) were exposed to clonidine (6.25–200 μM) and analyzed using comprehensive approaches. Key experiments includedviability assessment (eosin staining), motility evaluation Computer-Aided Sperm Analysis (CASA), intracellular calcium measurement, patch-clamp electrophysiology, mitochondrial membrane potential, reactive oxygen species quantification, capacitation analysis (chlortetracycline staining), and protein phosphorylation (Western blot). The results demonstrated that clonidine exhibited biphasic effects, where concentrations ≤ 50 μM preserved sperm viability and motility while inducing calcium responses, whereas concentrations ≥ 100 μM caused cytotoxicity. Most significantly, clonidine potently inhibited progesterone-induced calcium signaling, capacitation, and acrosome reaction while preserving spontaneous processes, and electrophysiological studies indicated partial Cation channel of Sperm (CatSper channel) enhancement with ∼50 % channel involvement in clonidine's calcium effects. Cation channel of Sperm (CatSper channel) enhancement with ∼50 % channel involvement in clonidine's calcium effects. These findings reveal that clonidine selectively interferes with progesterone-induced sperm responses while maintaining baseline functions, representing a novel mechanism affecting male fertility in vitro, which warrants further investigation regarding its potential clinical relevance.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109164"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145925610","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}

引用次数: 0

Unmasking hypoxia's double-edged sword: Mechanistic insights into granulosa cell adaptation and dysfunction 揭示缺氧的双刃剑：颗粒细胞适应和功能障碍的机制见解。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2026-02-05 DOI: 10.1016/j.reprotox.2026.109180

Ying Liu , Libing Ma , Yedan Gai , Jiwei Liu

{"title":"Unmasking hypoxia's double-edged sword: Mechanistic insights into granulosa cell adaptation and dysfunction","authors":"Ying Liu , Libing Ma , Yedan Gai , Jiwei Liu","doi":"10.1016/j.reprotox.2026.109180","DOIUrl":"10.1016/j.reprotox.2026.109180","url":null,"abstract":"<div><div>Granulosa cells are an important component of the ovary, surrounding the oocytes. The structural characteristics of ovarian follicles limit blood perfusion, thereby naturally forming an endogenous hypoxic microenvironment within the granulosa cell - oocyte complex. External hypoxic exposure (such as in high-altitude environments) further exacerbates the hypoxic condition of the ovary, making the regulation of low oxygen on the biological functions of granulosa cells a growing focus in reproductive biology and reproductive toxicology research. In this review, we systematically summarize and analyze the various impacts of hypoxia on the core physiological processes of granulosa cells (including proliferation, apoptosis, luteinization, and steroidogenesis), emphasizing the typical molecular signaling pathways that mediate these hypoxia-induced effects. We note that hypoxia is a double-edged sword in ovarian physiology: it regulates the adaptive physiological responses of granulosa cells to support normal follicle development, but excessive or persistent hypoxia can cause granulosa cell dysfunction and damage the development of ovarian follicles. Analyzing the exact hypoxia-mediated regulatory mechanisms in granulosa cells not only deepens our understanding of ovarian physiological homeostasis but also provides new insights into the mechanisms of hypoxia-related ovarian reproductive diseases.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109180"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137815","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}

引用次数: 0

Epigenetic dysregulation in idiopathic male infertility: The role of aberrant histone post-translational modifications 特发性男性不育症的表观遗传失调：异常组蛋白翻译后修饰的作用。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-03 DOI: 10.1016/j.reprotox.2025.109129

Jithin Biju , Suresh Kumar Raveendran , Kanive Parashiva Guruprasad , Aswath Kumar Reghunathan , Alex George

{"title":"Epigenetic dysregulation in idiopathic male infertility: The role of aberrant histone post-translational modifications","authors":"Jithin Biju , Suresh Kumar Raveendran , Kanive Parashiva Guruprasad , Aswath Kumar Reghunathan , Alex George","doi":"10.1016/j.reprotox.2025.109129","DOIUrl":"10.1016/j.reprotox.2025.109129","url":null,"abstract":"<div><div>Idiopathic male infertility (IMI), a condition with no clear clinical reason, represents a growing proportion of male reproductive complications. Traditional semen analysis fails to identify underlying etiology, leaving no indication for the sperm epigenome, particularly histone post-translational modifications which is emerging as a highly sensitive indicator of reproductive outcomes. This review synthesises evidence that different environmental toxicants such as chemical exposure, oxidative stress and lifestyle habits induce epigenetic alterations by disrupting histone post-translational modifications (HPTMs) in sperm. We critically evaluate how toxicant-induced dysregulation of critical HPTMs, serves as a key mechanism contributing to compromised spermatogenesis, poor sperm quality, and adverse reproductive outcomes. We explore the mechanisms through which specific toxicants alter the enzymatic machinery governing HPTM equilibrium. This comprehensive review highlights the utility of HPTMs as sensitive biomarkers of reproductive toxicity and underlines the urgent need for further research into the epigenetic mechanisms targeted by environmental contaminants to better assess reproductive risk and therapeutic strategies.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109129"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688099","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}

引用次数: 0

Maternal 3-NPA-induced oxidative stress impairs offspring ovarian function via glutamine metabolic dysregulation and NF-κB-mediated inflammation 母体3- npa诱导的氧化应激通过谷氨酰胺代谢失调和NF-κ b介导的炎症损害子代卵巢功能。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2026-01-07 DOI: 10.1016/j.reprotox.2026.109162

Lu Guo , Wenkai Yu , Bin Li , Xiaocheng Liu , Jiarong Zhang , Wenbin Tang

{"title":"Maternal 3-NPA-induced oxidative stress impairs offspring ovarian function via glutamine metabolic dysregulation and NF-κB-mediated inflammation","authors":"Lu Guo , Wenkai Yu , Bin Li , Xiaocheng Liu , Jiarong Zhang , Wenbin Tang","doi":"10.1016/j.reprotox.2026.109162","DOIUrl":"10.1016/j.reprotox.2026.109162","url":null,"abstract":"<div><div>Oxidative stress is a well-established contributor to reproductive dysfunction, yet its intergenerational effects on offspring ovarian health remain poorly understood. This study aimed to investigate whether 3-nitropropionic acid (3-NPA)-induced maternal oxidative stress impairs ovarian development in offspring and elucidate underlying mechanisms. Female C57BL/6 mice were intraperitoneally injected 3-NPA (40 mg/kg/day) for 21 days, while the control received saline. F1 offspring were assessed for ovarian function through follicle counts, serum FSH and AMH, and fertility metrics. Untargeted metabolomics and transcriptomics were performed on ovarian tissues, complemented by immunohistochemistry for glutamine metabolism enzymes of GLS1, GS, GDH and inflammatory markers (TNF-α). F1 offspring exhibited premature ovarian insufficiency (POI)-like phenotypes, including prolonged conception intervals, reduced pregnancy rates, elevated FSH, diminished primordial follicles and AMH levels, alongside impaired fertility. Maternal 3-NPA exposure induced sustained oxidative stress. Metabolomics revealed significant dysregulation of glutamine metabolism, with compensatory upregulation of GLS1/GS/GDH enzymes. Transcriptomics identified NF-κB/TNF-α pathway activation, validated by elevated ovarian TNF-α. Maternal oxidative stress triggers persistent ovarian dysfunction in offspring through glutamine metabolic disruption and NF-κB-mediated inflammation. This study provides the first evidence that 3-NPA induces intergenerational reproductive toxicity, highlighting glutamine metabolism and inflammatory pathways as potential targets for preventing oxidative stress-associated fertility decline.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109162"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145945708","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}

引用次数: 0

Ethylene oxide impairs sperm motility through dysregulation of Rab proteins 环氧乙烷通过Rab蛋白的失调损害精子活力

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2026-01-12 DOI: 10.1016/j.reprotox.2026.109168

Jae-Hwan Jo , Uwamahoro Claudine , Seung-Ik Jang , Eun-Ju Jung , Woo-Jin Lee , Jeong-Won Bae , Daehyun Kim , Joonho Moon , Seung Won Nam , Eu Jin Chung , Junkoo Yi , Woo-Sung Kwon

{"title":"Ethylene oxide impairs sperm motility through dysregulation of Rab proteins","authors":"Jae-Hwan Jo , Uwamahoro Claudine , Seung-Ik Jang , Eun-Ju Jung , Woo-Jin Lee , Jeong-Won Bae , Daehyun Kim , Joonho Moon , Seung Won Nam , Eu Jin Chung , Junkoo Yi , Woo-Sung Kwon","doi":"10.1016/j.reprotox.2026.109168","DOIUrl":"10.1016/j.reprotox.2026.109168","url":null,"abstract":"<div><div>Ethylene oxide (E.O) is an ether compound that negatively affects male reproduction, specifically by impairing sperm function. However, the molecular mechanisms underlying the E.O-induced inhibition of sperm function remain poorly understood. Therefore, this study investigated the molecular mechanisms behind E.O-induced toxic effects on sperm motility by assessing Ras-associated binding (Rab) proteins. Therefore, 31 individual Duroc semen samples were analyzed to determine the correlations between Rab protein (Rab3A, Rab5, Rab14, Rab25, Rab27A, and Rab34) levels and sperm motility after exposure to 100-μM E.O. The results showed that E.O exposure significantly reduced sperm motility and motion kinematics. Furthermore, correlation analysis revealed that, in the control group, Rab3A, Rab5, Rab14, Rab25, Rab27A, and Rab34 levels were correlated with various sperm motion parameters. In contrast, only Rab3A and Rab14 levels correlated with multiple sperm motility and kinematic parameters in the 100-μM-E.O group. These results suggest that E.O may affect sperm motion parameters via the action of Rab proteins, leading to decreased sperm motility. Consequently, these findings provide important evidence of the molecular mechanisms underlying E.O-induced toxic effects on sperm function.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109168"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977165","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}

引用次数: 0

Placental toxicity of alternative plasticizers: Current knowledge and future directions 替代增塑剂的胎盘毒性：目前的知识和未来的方向。

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-17 DOI: 10.1016/j.reprotox.2025.109143

Maira Nadeem, Michelle Jojy, Margaret Meschia, Genoa R. Warner

{"title":"Placental toxicity of alternative plasticizers: Current knowledge and future directions","authors":"Maira Nadeem, Michelle Jojy, Margaret Meschia, Genoa R. Warner","doi":"10.1016/j.reprotox.2025.109143","DOIUrl":"10.1016/j.reprotox.2025.109143","url":null,"abstract":"<div><div>Phthalates, a class of plasticizers, are known endocrine-disrupting chemicals that can negatively impact reproduction and development, including placental development and function. In response to growing concerns, various groups of chemicals, including but not limited to terephthalates, citrates, and cyclohexane dicarboxylic acids, have been developed as phthalate replacements. However, significant research gaps remain in understanding how these new chemicals affect humans. This review aims to synthesize existing research on how phthalate alternatives affect the placenta, a transient yet critical organ that supports fetal growth and development during pregnancy. Disruptions to placental structure and function can cause pregnancy complications and alter fetal programming. Herein, we review findings from biomonitoring, in vivo and in vitro experiments, as well as epidemiological studies to assess potential impacts. Although biomonitoring and house dust studies have identified the presence of alternative plasticizers, many identified chemical groups lack studies on their effects during pregnancy and on the placenta. Given the rising levels of these chemicals and their metabolites in urine and blood, further investigation into their mechanisms of toxicity is necessary. Notably, some alternatives may have the capability to alter pregnancy outcomes similar to traditional phthalates, such as by increasing the likelihood to develop conditions like gestational diabetes mellitus, although the majority of alternative plasticizers lack data. Understanding these impacts will inform public policy aimed at protecting maternal and fetal health, facilitate the development of safer consumer products, and prevent further emergence of regrettable replacements.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109143"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794614","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}

引用次数: 0

Maternal exposure to PM2.5 and its association with adverse pregnancy and birth outcomes: A prospective cohort study 产妇暴露于PM2.5及其与不良妊娠和分娩结局的关系：一项前瞻性队列研究

IF 2.8 4区医学

Reproductive toxicology Pub Date : 2026-03-01 Epub Date: 2025-12-04 DOI: 10.1016/j.reprotox.2025.109127

Garvita Parikh , Amiya Udayan Mehta , Niyamat Ali Siddiqui , Krishna Kumar , Mihir Adhikary , Bhoomika Patel

{"title":"Maternal exposure to PM2.5 and its association with adverse pregnancy and birth outcomes: A prospective cohort study","authors":"Garvita Parikh , Amiya Udayan Mehta , Niyamat Ali Siddiqui , Krishna Kumar , Mihir Adhikary , Bhoomika Patel","doi":"10.1016/j.reprotox.2025.109127","DOIUrl":"10.1016/j.reprotox.2025.109127","url":null,"abstract":"<div><h3>Background</h3><div>Maternal exposure to ambient air pollution is linked to various adverse pregnancy and birth outcomes (AP&BO). However, the association between particulate matter with a diameter of 2.5 μm (PM<sub>2.5</sub>) and AP&BO in India remains largely unexplored.</div></div><div><h3>Objective</h3><div>We aimed to investigate the association between PM<sub>2.5</sub> exposure and adverse pregnancy and birth outcomes in a prospective, hospital-based cohort study.</div></div><div><h3>Methods</h3><div>406 pregnant women aged 19–35, who were in their third trimester, were enrolled as per the inclusion/exclusion criteria. The study participants were divided into two groups according to their residential area’s air quality: Unexposed (203) and Exposed (203). A questionnaire was filled and 5 mL of umbilical cord blood and placental tissues were collected after delivery. Additionally, we analysed the systemic inflammatory markers (CRP, IL-6, TNF-α, and IL-1β) in the cord blood and the presence of black carbon in 50 placental tissue samples.</div></div><div><h3>Results</h3><div>Each 10 µg/m<sup>3</sup> increase in PM<sub>2.5</sub> had a statistically significant relation with pre-eclampsia, preterm labor, preterm birth, low birth weight, and small for gestational age, even after accounting for possible confounders. A statistically significant association between CRP, IL-6, TNF-α, and IL-1β, with each 10 µg/m³ increase of PM<sub>2.5,</sub> was observed. Black carbon (BC) deposition was detected at the foetal side of the placenta only in the exposed group.</div></div><div><h3>Conclusion</h3><div>Our study indicates that maternal exposure to increased levels of PM<sub>2.5</sub> during the third trimester is associated with an increased risk for AP&BO.</div></div>","PeriodicalId":21137,"journal":{"name":"Reproductive toxicology","volume":"140 ","pages":"Article 109127"},"PeriodicalIF":2.8,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145692210","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}

引用次数: 0