Search Results (366)

Particulate atmospheric pollution poses a global threat to human health. Metals enter the body through inhalation attached to these particles. Certain vulnerable groups are more susceptible to toxicity because of age, physiological changes, and chronic and metabolic diseases and also workers because of high and cumulative exposure to metals. A narrative review was conducted to examine the effects of key metals—arsenic, cadmium, chromium, copper, lead, mercury, manganese, nickel, vanadium, and zinc—on vulnerable populations, analyzing articles published over the past decade. Some of these metals are essential for humans; however, excessive levels are toxic. Other non-essential metals are highly toxic. Shared mechanisms of toxicity include competing with other minerals, oxidative stress and inflammation, and interacting with proteins and enzymes. Prenatal and childhood exposures are particularly concerning because they can interfere with neurodevelopment and have been associated with epigenetic changes that have long-term effects. Occupational exposure has been studied, but current exposure limits for specific metals appear dangerous, emphasizing the need to revise these standards. Older adults, pregnant women, and individuals with metabolic diseases are among the least studied groups in this review, underscoring the need for more research to understand these populations better and create effective public health policies. Full article

The proper course of pregnancy and fetal development depends, among other factors, on maintaining adequate levels of micronutrients in the maternal body. This integrative, concept-driven narrative review summarizes the current state of knowledge on the impact of selected elements, referred to as oncoelements, on placental function and obstetric outcomes. These include both potentially protective elements (selenium, zinc, copper) and toxic metals (cadmium, lead, arsenic), which, in excess may disrupt oxidative, hormonal, and epigenetic homeostasis. Rather than providing a quantitative synthesis, the article is structured around a four-level conceptual model integrating molecular mechanisms, placental protection, clinical outcomes, and umbilical cord blood as a biomarker of prenatal exposure. Mechanisms of toxicity include oxidative stress, mitochondrial dysfunction, DNA damage, and altered gene expression. Given the observational nature of most studies, clinical recommendations remain cautious. Micronutrient assessment may be useful in selected high-risk groups, but requires further validation. In environmentally burdened regions, screening for toxic metals may be considered. Future research should clarify dose–response relationships, define threshold concentrations, and explore molecular biomarkers of exposure. Umbilical cord blood offers a promising matrix for assessing fetal exposure, although interpretation is limited by methodological variability and the lack of reference values. Full article

Developmental programming, shaped by environmental and lifestyle stressors during prenatal life, is increasingly recognized as a major contributor to non-communicable diseases (NCDs) later in life. Oxidative stress, one of key mechanisms linking these stressors to fetal metabolomic reprogramming and disease pathogenesis, leaves measurable metabolomic signatures that reflect disrupted redox balance. Alterations in glucose, lipid, and amino acid metabolism and antioxidant response could reveal the main pathways driving NCD development. This review summarizes epidemiological studies that have investigated biochemical responses of the prenatal exposure to metals, air pollution, and tobacco smoke and e-cigarette vapor in maternal–placental–fetal compartments using a metabolomic approach. Summarized studies indicate that maternal exposure to metals primarily disrupts amino acid pathways related to one-carbon metabolism, glutathione synthesis, and oxidative stress defense, while air pollution, particularly fine particulate matter, mainly affects lipid oxidation, fatty acid β-oxidation, and amino acid and carbohydrate metabolism. Tobacco smoke and e-cigarette vapor induce widespread disturbances involving reduced citric acid cycle intermediates, altered acylcarnitines and phospholipids, and impaired antioxidant capacity, collectively promoting oxidative damage and inflammatory signaling. The identification of these metabolome alterations might contribute to a deeper understanding of the toxicity and biological impact of environmental stressors on offspring health. These results may eventually lead to the identification of early biomarkers and to the development of therapeutic strategies aimed at reducing NCD risk. Full article

Gestational obesity, defined as obesity during pregnancy or a pre-pregnancy BMI ≥30, is a growing global health challenge with profound implications for both maternal and offspring health. This narrative review synthesizes current evidence on the mechanistic pathways by which maternal obesity affects pregnancy outcomes and intergenerational health trajectories. For mothers, gestational obesity increases the risk of gestational diabetes, hypertensive disorders, cesarean delivery, and postpartum weight retention. Offspring exposed to maternal obesity face higher risks of obesity, metabolic syndrome, cardiovascular disease, and neurodevelopmental disorders, many of which persist across the lifespan. The underlying mechanisms include metabolic dysregulation, insulin resistance, chronic inflammation, oxidative stress, and alterations in placental function. Epigenetic modifications, such as DNA methylation, histone changes, and non-coding RNA expression, play central roles in fetal programming, while maternal gut dysbiosis and alterations in breast milk microbiota further shape infant health outcomes. Importantly, maternal obesity not only influences pregnancy and early life but also perpetuates an intergenerational cycle of obesity and related comorbidities. Preventive strategies targeting preconception and prenatal health, combined with interventions to optimize lactation and maternal diet, may mitigate long-term risks. Future research should prioritize longitudinal and mechanistic studies to refine interventions aimed at disrupting the transmission of obesity-related disease across generations. Full article

Background: Prenatal depression, affecting up to a quarter of all pregnancies in the United States, contributes to morbidity and mortality and is associated with increased risk of adverse birth and long-term mental health outcomes. Adverse childhood experiences (ACEs, or experiences of abuse, neglect, or family dysfunction experienced prior to age 18) are a strong predictor of adult depression and adverse health outcomes. The present study investigated whether epigenetic modification in the form of DNA methylation (DNAm) of four stress-related, glucocorticoid pathway genes (CRH, CRHR1, FKBP5, NR3C1) mediates associations between ACEs and depressive symptoms among Black pregnant women. Methods: Using a cross-sectional design, we examined the mediating role of DNAm on the relationship between depressive symptoms (Center for Epidemiologic Studies Depression Scale (CES-D)) and ACEs (Centers for Disease Control and Prevention 10-item questionnaire), in a subsample (n = 61) of Black pregnant women who were participants of the Biosocial Impacts of Black Births (BIBB) study. Results: A significant association was found between ACEs and depressive symptoms scores (TE α_X = 2.29 with p_TE = 6.60 × 10⁵). DNAm on five CpG sites within two genes significantly mediated the relationship between ACEs and depressive symptoms (cg03238273 on CRHR1, and cg08845721, cg16594263, cg19820298, and cg23430507 on NR3C1). Conclusions: This study provides evidence that DNAm partially mediated the association of ACEs and depressive symptoms during pregnancy among Black pregnant women. Understanding the molecular pathways underlying the mediating effect of ACEs on depressive symptoms among Black pregnant women can illuminate biological markers that help identify and treat pregnant women who are at an increased risk for depression following childhood trauma. Full article

Prenatal ozone (O₃) exposure may trigger systemic inflammation and oxidative stress. These effects could contribute to adverse pregnancy outcomes. We conducted a prospective cohort study involving 235 pregnant women in Ningxia, China. Maternal O₃ exposure during pregnancy and prior to conception was assessed using high-resolution spatiotemporal models. Multivariable logistic and linear regression analyses were employed to evaluate the associations between O₃ exposure and adverse pregnancy outcomes. Mediation and interaction models were further applied to examine the potential modifying roles of gestational diabetes mellitus (GDM) and inflammatory biomarkers. In multivariable analyses adjusted for maternal and environmental covariates, higher prenatal O₃ exposure was significantly associated with an increased risk of preterm birth (PTB) (OR = 1.24, 95% CI: 1.05~1.45, p = 0.010) and low birth weight (LBW) (OR = 1.29, 95% CI: 1.09~1.54, p = 0.004). Similarly, elevated maternal SAA and CRP levels were positively associated with these adverse pregnancy outcomes (p < 0.05). Notably, higher TNF-α levels were inversely associated with the risks of PTB (OR = 0.15, 95% CI: 0.03~0.85, p = 0.032) and LBW (OR = 0.05, 95% CI: 0.01~0.39, p = 0.005). IL-17A levels were inversely associated with neonatal length-for-age Z scores (β = −0.28, 95% CI: −0.55~−0.01, p = 0.043). Our findings suggest that prenatal O₃ exposure is associated with increased risks of PTB and LBW. Alterations in systemic inflammatory markers and metabolic dysfunction during pregnancy were related to adverse pregnancy outcomes and fetal growth deficits, but they did not mediate these associations, with O₃ remaining an independent predictor after adjustment. Full article

Chronic exposure to structural violence and environmental hazards may disrupt stress regulation, trigger inflammation, and impair iron metabolism in women. Iron deficiency has been associated with depression, but the combined impact of environmental stressors and anemia on maternal mental health remains understudied. We analyzed associations between 28 neighborhood-level environmental stressors, hemoglobin levels, and depressive symptoms (measured by the Patient Health Questionnaire-9) during early pregnancy, using retrospective data from 1964 pregnant patients (2015–2019) at an urban health center in Chicago. Demographic and residential data were linked to environmental indicators from the Chicago Health Atlas. Factor analysis reduced the environmental variables, and multivariable regression models examined associations with PHQ-9 scores at first pregnancy encounter. Participants were predominantly non-Hispanic Black (56%) and Hispanic (27%), with 13% anemic and 16% screening positive for depressive symptoms. Poverty, non-Hispanic Black race, single status, public or no insurance, and unemployment were associated with higher depressive symptoms. Among anemic individuals, neighborhood crime was significantly associated with depressive symptoms, while hemoglobin levels and gestational age were not. These findings highlight how environmental and social inequities contribute to maternal mental health disparities and support the need for integrated, equity-focused prenatal care interventions. Full article

Background: Prenatal stress affects fetal neurodevelopment and may increase the risk of seizures. This study aimed to analyze the impact of maternal restraint stress during pregnancy on neonatal status epilepticus (SE) in rats. Methods: Pregnant Wistar rats were subjected to restraint stress from gestation days 12 to 20. Offspring were assessed for body weight, size, and corticosterone levels. SE was induced in postnatal day 7 rats using the lithium–pilocarpine model. Neurodegeneration was analyzed using Fluoro-Jade C staining. Results: Maternal restraint stress resulted in reduced weight gain for the mothers and lower body weight and size for their offspring. Stressed neonates exhibited higher levels of serum corticosterone. Male neonates exhibited shorter latency to stage 1 seizures and increased hippocampal neurodegeneration compared with control males, whereas female neonates were largely unaffected. Conclusions: Maternal restraint stress produced only mild, sex-dependent effects on neonatal seizure susceptibility, affecting males but not females, suggesting a limited yet selective influence of prenatal stress on early brain vulnerability. Full article

Neurodevelopmental disorders (NDDs), including autism spectrum disorder, intellectual disability, and attention deficit hyperactivity disorder, are increasingly recognized as disorders of early brain construction arising from defects in neural stem and progenitor cell (NSPC) proliferation. NSPCs are responsible for generating the diverse neuronal and glial lineages that establish cortical architecture and neural circuitry; thus, their expansion must be tightly coordinated by intrinsic cell cycle regulators and extrinsic niche-derived cues. Disruption of these mechanisms—through genetic mutations, epigenetic dysregulation, or environmental insults—can perturb the balance between NSPC self-renewal and differentiation, resulting in aberrant brain size and connectivity. Recent advances using animal models and human pluripotent stem cell-derived brain organoids have identified key signaling pathways, including Notch, Wnt, SHH, and PI3K–mTOR, as central hubs integrating proliferative cues, while transcriptional and chromatin regulators such as PAX6, CHD8, SETD5, and ANKRD11 govern gene expression essential for proper NSPC cycling. Furthermore, prenatal exposure to teratogens such as Zika virus infection, valproic acid, or metabolic stress in phenylketonuria can recapitulate proliferation defects and microcephaly, underscoring the vulnerability of NSPCs to environmental perturbation. This review summarizes emerging insights into the molecular and cellular mechanisms by which defective NSPC proliferation contributes to NDD pathogenesis, highlighting convergence among genetic and environmental factors on cell cycle control. A deeper understanding of these pathways may uncover shared therapeutic targets to restore neurodevelopmental trajectories and mitigate disease burden. Full article

Maternal immune activation (MIA) is a recognized environmental risk factor for altered brain development, yet its early molecular consequences remain unclear. In this study, we examined total Tau, site-specific Tau phosphorylation, and selected synaptic proteins in one-month-old female mouse offspring exposed prenatally to MIA evoked by poly(I:C), a synthetic mimetic of viral dsRNA. Our analyses revealed a consistent reduction in Tau phosphorylation at Ser416 across multiple brain regions, including the cortex, hippocampus, and cerebellum, without changes in total Tau levels or other phosphorylation sites. Among synaptic markers, only Shank3 levels were decreased, and this effect was confined to the cerebellum. No additional robust alterations were detected at this stage of development. These findings suggest that Tau hypophosphorylation at Ser416 may represent an early and widespread molecular footprint of MIA, whereas cerebellar Shank3 downregulation points to a region-specific vulnerability of synaptic pathways. While the study is limited to female offspring and a single postnatal time point, the data provide new insights into subtle molecular signatures that could precede or accompany later functional outcomes. Our results highlight Tau phosphorylation and Shank3 expression as potential molecular markers of prenatal immune stress, warranting further longitudinal and sex-comparative studies to clarify their relevance for neurodevelopmental trajectories. Full article

Maternal stress during gestation can alter offspring physiology, behaviour, and immune function. In pigs, such ‘prenatal stress’ is known to increase stress sensitivity, but the potential to automatically detect such sensitivity has remained unexplored. Automatic detection of facial expression has successfully identified differences in pigs dependent on their stress status. This study progresses this work by demonstrating that, for the first time, using a deep learning framework applied to facial analysis, stress-linked phenotypes can be learned from one generation and detected in the next. Using a dataset of over 7000 facial images from 18 gestating sows and 53 of their daughters, we trained and evaluated five state-of-the-art deep learning architectures across six independent daughter cohorts. Attention-based models significantly outperformed CNN-based models, with the Vision Transformer (ViT) model achieving a mean accuracy of 0.78 and an average F1-score of 0.76. Grad-CAM visualisations showed that the ViT consistently attended to biologically relevant facial regions, such as the eyes and snout, whereas CNNs often focused on diffuse or non-informative areas, resulting in reduced low-stress recall and greater batch sensitivity. Models trained on maternal facial images successfully predicted stress responsiveness in daughters from unrelated lineages, indicating that the model captured generalisable facial cues of stress rather than familial resemblance. This approach supports previous work showing that machine vision can detect putatively stress-related alterations to facial expression in pigs. Future application of this approach could offer a scalable, non-invasive tool for early detection of stress in livestock production systems, opening new avenues for welfare-oriented precision livestock management and informed breeding strategies aimed at improving stress resilience. Full article

Prenatal maternal stress (PS) is a risk factor for adverse offspring neurodevelopment. Heart rate variability (HRV) complexity provides a non-invasive marker of maternal autonomic regulation and may be influenced by mind–body interventions such as Yoga. In this quasi-randomized controlled trial, 28 chronically stressed pregnant women were followed from the second trimester until birth: 14 participated in weekly Hatha Yoga with electrocardiogram (ECG) recordings, and 14 received standard obstetric care with monthly ECGs. Group allocation was based on availability, with participants unaware of their assignment at enrollment. HRV complexity was assessed first with Sample Entropy and Entropy Rate and then expanded to 94 HRV metrics spanning temporal, frequency, nonlinear, and information-theoretical domains. All metrics were covariate-adjusted (maternal age, BMI, gestational age), standardized, and analyzed using timepoint-specific principal component analysis (PCA). From this, a unified HRV index was derived. Analyses revealed that HRV metric relationships changed dynamically across pregnancy, with PCA loadings shifting from frequency toward complexity measures in late gestation. The mixed effects model identified a significant time x group interaction effect (p = 0.041). These findings suggest a restructuring of HRV signal-analytical domains with advancing pregnancy attributable to Yoga and highlight the utility of advanced HRV analysis frameworks for future, larger trials. Full article

Environmental stressors during the crucial period of fetal development can have a substantial impact on long-term health outcomes. A major concern is dietary exposure to endocrine-disrupting chemicals (EDCs), which can readily cross the placenta and disrupt fetal hormonal signaling and developmental programming. Examples of these chemicals include bisphenols, phthalates, pesticides, and persistent organic pollutants (POPs). Prenatal exposure to EDC has been associated with long-term effects in children, including immune disruption, metabolic dysregulation, impaired neurodevelopment, and reproductive alterations, as evidenced by human cohort studies and experimental models. Epigenetic reprogramming, direct interference with endocrine signaling, and oxidative stress (OS) are hypothesized pathways for these adverse consequences, which often combine to produce long-lasting physiological changes. This narrative review summarizes current research on maternal dietary exposure to EDCs during pregnancy, highlighting associations with adverse child health outcomes. It also discusses the growing evidence of transgenerational effects, the potential mechanisms linking prenatal exposure to long-term outcomes, and the importance of understanding the roles of timing, dosage, and chemical type. By highlighting the necessity of focused interventions to lower maternal EDC exposure and lessen threats to the health of offspring, the review concludes by discussing implications for future research, preventive measures, and public health policy. Full article

Prenatal physical activity (PA) has well-established benefits for maternal mental health. However, PA levels are generally low among pregnant individuals and were even lower during the COVID-19 pandemic. Since walking is the most popular form of prenatal PA, we aimed to examine associations between walking in the third trimester of pregnancy and mental health symptoms of depression, anxiety, pregnancy-related anxiety and perceived stress during the pandemic. Relevant pandemic-related factors (e.g., COVID-19 waves, population density) associated with walking were also studied. Pregnant individuals were recruited across Quebec (Canada) between October 2020 and September 2022, as part of the Resilience and Perinatal Stress during the Pandemic (RESPPA) study. Analyses were conducted on data collected via online questionnaires during the third trimester (n = 1086). Results revealed that higher levels of walking were significantly associated with lower symptoms of generalized anxiety (β = −0.06, p = 0.035), and perceived stress (β = −0.07, p = 0.007). Living in a more densely populated area, living with fewer children at home and having a university degree were associated with higher levels of walking. Those who completed their questionnaire in the second pandemic wave also reported higher levels of walking. Our results highlight the potential of walking in the third trimester to support maternal mental health. Full article

In recent years, increasing attention has been paid to the impact of air pollution on the neuropsychological development of children and adolescents. However, a comprehensive overview of global research trends and thematic structures in this field remains lacking. This study applies bibliometric methods to systematically analyze 1441 English-language publications from 2000 to 2024, retrieved from the Web of Science Core Collection and Scopus. Using CiteSpace 6.4.R1, VOSviewer 1.6.20, and RStudio Bibliometrix (RStudio version: 2025.05.1+496, R version: 4.5.0, Bibliometrix package version: 5.0.0), we conducted a multidimensional visualization of publication trends, contributing countries and institutions, interdisciplinary integration, author collaborations, and keyword clustering. Results show a marked increase in research output in recent years, with the United States, China, and Spain leading in publication number and international collaboration. Key research themes include particulate pollution, prenatal and early-life exposure, and neuropsychological disorders such as attention-deficit hyperactivity and autism, alongside mechanisms like oxidative stress and neuroinflammation. This study builds a knowledge framework for the field, offering insights for scholars and evidence-based guidance for policymakers to support interventions that protect the neuropsychological health of the younger population. Full article