Search Results (338)

Background/Objectives: The pre-diagnosis dietary intake in newly diagnosed multi-ethnic paediatric inflammatory bowel disease (PIBD) is not well understood. This study aimed to describe the pre-diagnosis diet and environmental factors in children with newly diagnosed PIBD attending a single Australian tertiary children’s hospital. Methods: A pilot cross-sectional study was conducted from February 2022 to February 2023 involving children with newly diagnosed PIBD. Results: Of 56 children confirmed with PIBD, 54% had Crohn’s disease (CD)—mean ± SD age, 11.55 years ± 2.84—and 46% had Ulcerative Colitis (UC)—11.50 years ± 2.94 (45%, non-Caucasian). More Caucasians had an IBD family history (48.3% vs. 20%; p = 0.02 *). Non-Caucasian children demonstrated significantly lower mean serum vitamin D levels than Caucasian children (42.5 vs. 69 nmol/L; p ≤ 0.001 ***). Most children across ethnicities for both IBD subtypes had ‘regular’ intakes of red meat, whereas more Caucasian children had ‘regular’ intakes of processed/deli meat (72% vs. 39%; p = 0.02 *). A total of 64% of non-Caucasian children with CD reported a usual pre-diagnosis diet that differed from the traditional diet, compared to 42% with UC (p = 0.29). When eating out, fast foods were chosen regularly by most children with PIBD. Pre-diagnosis dietary intake data indicated that most with PIBD ‘rarely/never’ had whole-food sources of plant protein and had ‘infrequent’ intake of rice. Plant food diversity was low (mean 11 types/week). Conclusions: The significantly lower likelihood of IBD family history, along with relatively lower vitamin D levels, and the predominance of a Western-style dietary pattern among non-Caucasian children are compatible with the hypothesis that non-genetic factors may be important in PIBD, warranting further investigation into diet and environmental factors in this group. Further investigation of the pre-disease modifiable non-genetic factors contributing to the development of PIBD in the migrant population group is recommended. The finding across ethnicities of low pre-diagnosis plant food diversity was novel; however, due to the lack of healthy controls and the use of a novel but non-validated exposome tool, causality associations should be interpreted cautiously. Full article

Air pollution represents a critical yet modifiable factor influencing the recurrence and progression of upper-airway infections. This review explores the molecular, immunological, and environmental mechanisms linking airborne pollutants to recurrent sinus and respiratory tract inflammation. Particular focus is placed on pollutant-induced oxidative stress, epithelial barrier disruption, alterations in the microbiome, and immune dysregulation, which collectively heighten disease susceptibility. Integrating recent advances in exposomics, multi-omics, and artificial intelligence, the discussion highlights new approaches to unravel exposure–response pathways and identify predictive biomarkers. Future directions emphasize precision exposure assessment, interventional strategies to improve air quality, and the emerging framework of “clean-air medicine” to guide prevention and policy. Overall, this synthesis underscores the urgent need for multidisciplinary collaboration across environmental science, molecular biology, and clinical research to mitigate the growing burden of pollution-related airway disease and promote sustainable respiratory health. Full article

Accounting for over 1.2 million new diagnoses worldwide in 2022, non-melanoma skin cancer (NMSC) represents the most common human cancer, predominantly manifesting as basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). NMSC serves as a powerful natural model for studying how environmental exposure, the exposome, reprograms the epigenome to drive carcinogenesis. Chronic ultraviolet radiation (UVR), the dominant risk factor, induces DNA damage and inflammation that dysregulate epigenetic enzymes (e.g., DNMTs, HDACs). These effects are layered with perturbations from β-HPV infection and cutaneous dysbiosis, altering DNA methylation, histone modifications, and non-coding RNA and miRNA expression in a multistep carcinogenic process. This review synthesizes the central role of epigenetic regulation as the critical interface between genetic susceptibility and cumulative exposome factors in NMSC pathogenesis. We integrate how UVR, HPV, and inflammation converge to remodel the keratinocyte epigenome. Finally, we evaluate the translational potential of this knowledge for refined risk stratification through epigenetic biomarkers and discuss emerging therapeutic strategies, including epidrugs, that target these dysregulated pathways for advanced NMSC management. Full article

Environmental pollutants, lifestyle factors, and intrinsic metabolism can amplify reactive oxygen and nitrogen species (ROS/RNS) generation beyond antioxidant capacity. The resulting oxidative stress damages macromolecules, perturbs redox signaling, and may accelerate biological aging. This review synthesizes evidence published mainly in 2020–2025 on how major pollutant classes (air pollutants, metals, pesticides, nanoparticles, and micro-/nanoplastics) induce ROS through shared nodes mitochondrial electron transport disruption, NADPH oxidase activation, and redox cycling/Fenton chemistry and how these signals propagate to epigenetic remodeling (DNA methylation, histone modifications, and non-coding RNAs). To move beyond descriptive cataloging, we grade the strength of evidence by study context (cell culture, animal models, human observational studies, and clinically oriented biomarker research), highlight convergent findings and unresolved controversies, and specify key methodological limits. We then compare oxidative-stress biomarker platforms by analytical specificity, pre-analytical susceptibility, and translational readiness, distinguishing validated markers from exploratory redox-epigenetic and multi-omics signatures. Finally, we discuss how exposomics and AI-assisted multi-omics integration may support biomarker discovery while emphasizing current constraints (confounding, batch effects, and limited prospective validation) that must be addressed for clinical translation. Full article

Background: Dermatological conditions represent a leading cause of global nonfatal disease burden, accounting for approximately 42.9 million disability-adjusted life years annually. Their complex pathogenesis is increasingly understood through the skin–brain–exposome axis, a bidirectional neuroimmunological and environmental communication network. The study aims to synthesize the neurobiological mechanisms of the skin–brain–exposome axis with macroscopic sociodemographic modifiers, clinical manifestations, and evidence-based psychodermatological interventions. Methods: A narrative review was conducted, following a structured search of PubMed, Scopus, and Web of Science (from inception to February 2026), yielding 54 sources. Mechanistic and interventional data (including randomized controlled trials and meta-analyses) were integrated with large-scale population-based epidemiological findings, anchored by a recent cross-sectional Polish cohort of 27,000 adults. Results: Psychological distress is associated with hyperactivation of the hypothalamic–pituitary–adrenal (HPA) axis and peripheral neurogenic inflammation (e.g., Substance P, corticotropin-releasing hormone), exacerbating stress-sensitive conditions such as atopic dermatitis, psoriasis, acne, and chronic pruritus. External exposome factors (urbanization, pollution) and sociodemographic variables (education, gender) may modify biological risk and diagnostic capture rates, frequently generating an epidemiological diagnostic paradox. Randomized trials support that psychotherapeutic interventions, particularly Cognitive Behavioral Therapy (CBT) and Mindfulness-Based Stress Reduction (MBSR), effectively disrupt the physical itch–scratch–stress cycle and improve disease-specific quality of life, serving as evidence-based adjunctive strategies in comprehensive care. Conclusions: Effective dermatological management requires targeting both the cutaneous barrier and the psychological exposome. Integrating routine psychosocial screening and stratified behavioral interventions into standard clinical care is essential for addressing the neuroimmune chronicity of inflammatory skin diseases. Full article

Background: Per- and polyfluoroalkyl substances (PFAS) represent a large class of synthetic fluorinated compounds characterized by highly stable carbon–fluorine bonds that confer exceptional environmental persistence and bioaccumulative properties. Although regulatory measures have restricted the production of several PFAS, including perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), their environmental persistence continues to maintain widespread human exposure, while newly introduced replacement compounds raise additional toxicological concerns. Notably, the recent evidence demonstrating PFAS-induced alterations in key cardiac ion channel activity and electrocardiographic parameters suggest potential electrophysiological mechanisms that may contribute to arrhythmogenesis and cardiac arrhythmias including the most frequent one, atrial fibrillation (AF). Methods: We conducted a narrative literature review of experimental, epidemiological, and mechanistic studies investigating and reporting the cardiovascular, electrophysiological, and potential arrhythmogenic effects of PFAS. Results: Available evidence indicates that PFAS exposure is associated with alterations in cardiac electrophysiology, including modulation of ion channel activity (notably sodium, calcium, and potassium channels), disruption of calcium handling, and changes in electrocardiographic parameters such as QT interval prolongation, which are key contributors to arrhythmogenesis and AF. Conclusions: This review highlights the need for improved understanding of PFAS-induced electrophysiological alterations, to clarify the role of PFAS in cardiac arrhythmias including AF. Full article

A comprehensive ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) method was developed for the simultaneous quantification of 50 pesticide biomarkers across nine current-use chemical classes in human urine. These classes include organophosphorus insecticides (which encompass dialkyl phosphates and specific metabolites), pyrethroid insecticides, fungicides, neonicotinoid insecticides, herbicides, insect repellents, organochlorine pesticide metabolites, and plant growth regulators. The method employs solid-phase extraction (SPE) for sample preparation, requiring only 0.2 mL of urine. Chromatographic separation was optimized using a Hypersil Gold AQ column, achieving a total run time of 18 min. Mass spectrometric detection utilized polarity switching in electrospray ionization mode with multiple reaction monitoring. Method validation demonstrated satisfactory linearity (R² > 0.99), high sensitivity with limits of detection ranging from 0.01 to 0.88 ng/mL, and extraction efficiencies between 85% and 113%. Precision and accuracy were within acceptable ranges, with relative standard deviations generally below 15%. The method’s robustness was confirmed through participation in external quality assessment schemes. Application to real samples revealed significant inter-individual variability in pesticide biomarker concentrations, with total measured biomarker levels ranging from 89 to 1242 ng/mL across the 10 individuals analyzed. This method offers comprehensive coverage of current-use pesticide chemical classes, including 30 biomarkers from the U.S. National Health and Nutrition Examination Survey (NHANES) biomonitoring program, and demonstrates improved sensitivity and broader analyte coverage compared to existing methods. The developed assay provides a valuable tool for large-scale biomonitoring studies and environmental health research. Full article

Nanoplastics (NPs, <100 nm) have emerged as nano-scale contaminants with superior mobility and biological barrier-crossing capacity, yet risk assessment fails due to unstandardized analytical methods and a lack of realistic exposure data. This perspective proposes an “Exposome–Microbiome–Immune” (EMI) framework as a One Health paradigm to integrate detection, toxicokinetics, and systemic effects. We prioritize the following actions: (i) validated nano–Fourier transform infrared spectroscopy (nanoFTIR) and surface-enhanced Raman spectroscopy (SERS) for environmental/human monitoring; (ii) multigenerational studies in zebrafish and organoids; (iii) longitudinal cohorts for biomonitoring. Without shifting from descriptive reviews to systems toxicology, NP risk will remain underestimated. Full article

Micro- and nanoplastics (MPs/NPs) have emerged as pervasive environmental contaminants with increasing implications for human health, particularly within the digestive system. This review critically examines the role of MPs/NPs as disruptors of gastrointestinal and liver homeostasis through the lens of the plastic–gut–liver axis. We synthesize current evidence on primary exposure routes—including ingestion, inhalation, dermal contact, and transplacental transfer—and highlight their intestinal uptake, systemic dissemination, and tissue accumulation. Mechanistically, MPs/NPs compromise intestinal barrier integrity, promote oxidative stress, and induce microbiota dysbiosis, facilitating the translocation of microbial-derived signals to the liver via the portal circulation. This process triggers inflammatory signaling cascades, metabolic reprogramming, and immune dysregulation, contributing to hepatic steatosis, insulin resistance, and potential carcinogenic processes. Emerging evidence also implicates pancreatic dysfunction and β-cell stress within a broader gut–liver axis context. We further discuss the systemic propagation of MPs/NPs-induced dysbiosis along multi-organ axes, including gut–lung and gut–brain interactions. Despite robust preclinical data, human evidence remains limited due to methodological heterogeneity and the lack of standardized biomarkers. This review underscores critical knowledge gaps and emphasizes the need for integrative, translational approaches to clarify long-term health risks and inform regulatory strategies within the environmental exposome framework. Full article

Background: Human lead exposure is a multi-pathway phenomenon that integrates internal biological burden with persistent residential environmental reservoirs. Although individual lead metrics have been linked to cardiometabolic dysfunction, current research often fails to capture the ‘exposome’ reality of joint, nonlinear, and interaction-dependent effects on metabolic outcomes like BMI. Objectives: To evaluate associations between biological (blood and urinary) and residential dust (window and floor) lead measures and BMI, and to characterize nonlinear and interaction-dependent mixture effects using Bayesian Kernel Machine Regression (BKMR). Methods: We analyzed data from NHANES 2001–2002, a nationally representative survey of the U.S. noninstitutionalized civilian population. Window and floor dust lead (µg/ft²) were obtained from the NHANES household dust component, and blood lead (µg/dL) and urinary lead (µg/L) were measured using standardized NHANES laboratory protocols. BMI was calculated from measured height and weight. Missing data were addressed using multivariate imputation by chained equations. Descriptive statistics and multivariable linear regression were used to estimate adjusted associations between individual lead metrics and BMI, controlling for age, gender, income, race/ethnicity, and education. BKMR was then applied to evaluate joint mixture effects, estimate univariate and bivariate exposure–response functions, and quantify relative exposure importance using posterior inclusion probabilities (PIPs). Results: In covariate-adjusted linear regression, blood lead (β = −0.485; 95% CI: −0.566, −0.405; p < 0.001) and window dust lead (β = −0.00047; 95% CI: −0.00067, −0.00026; p < 0.001) were inversely associated with BMI, whereas floor dust lead was positively associated (β = 0.258; 95% CI: 0.209, 0.306; p < 0.001). Urinary lead was inversely but not significantly associated with BMI (β = −0.111; 95% CI: −0.235, 0.013; p = 0.079). In BKMR, blood lead was the dominant contributor, with a posterior inclusion probability (PIP; proportion of iterations in which an exposure is selected) of 1.00. Window dust lead showed modest inclusion (PIP = 0.26), whereas urinary and floor dust lead were not selected (PIP = 0.00). Exposure–response functions indicated modest nonlinearity for blood lead and greater divergence for the blood lead–window dust lead pairing at higher exposure levels. The overall mixture effect declined across increasing joint exposure quantiles, crossing the null near the median and becoming increasingly negative at higher mixture levels. Conclusions: In our study, lead metrics showed heterogeneous associations with BMI, and BKMR indicated that internal lead burden (blood lead) primarily drove mixture-related BMI patterns, with evidence that window dust lead may modify mixture effects at higher co-exposure levels. These findings support evaluating multiple lead exposure pathways jointly and using flexible mixture models to capture nonlinear and interaction-dependent relationships with BMI. Full article

Background: Brain-derived neurotrophic factor (BDNF) is central to synaptic plasticity and neurodevelopment. Toxic metal exposure is linked to oxidative stress and neuroinflammation, yet its effects on BDNF signaling remain unclear. Objectives: To systematically synthesize evidence from human and experimental studies on the association between environmental or occupational metal exposure and BDNF alterations, and to highlight research gaps with an emphasis on hexavalent chromium (Cr(VI)). Methods: PubMed, Scopus, and ScienceDirect were searched following PRISMA guidelines. Eligible studies included human observational research and animal models reporting quantitative associations between metal exposure (biomarkers/environmental measures) and BDNF outcomes (protein or gene expression). Data were extracted on exposure assessment, BDNF measurement, and neurobehavioral outcomes. Study quality was assessed using NOS (human studies) and SciRAP (experimental studies). Results: Nineteen studies were included. Across metals such as Pb, Hg, Cd, As, Mn, and mixtures, exposure was associated with altered BDNF levels in blood or brain tissue, often alongside oxidative stress markers, inflammatory changes, and cognitive or behavioral impairment in animal models. Most human studies reported decreased circulating BDNF with higher exposure, while experimental evidence suggested context-dependent regulation across exposure windows and brain regions. Conclusions: The available evidence supports a biologically plausible link between metal exposure and BDNF dysregulation. No eligible studies evaluated BDNF in relation to Cr(VI), indicating a major research gap. Future studies should integrate neurotrophic biomarkers with exposome-oriented designs to clarify chromium-related neurotoxicity and support Adverse Outcome Pathway (AOP)-informed frameworks. Full article

Cosmetic dermatology has largely focused on topical applications targeting the stratum corneum. However, emerging evidence suggests that visible aging is a systemic readout of internal “organ clocks” and molecular dysregulation across the epidermis and dermis. This review proposes an “inside–out strategy” that seeks to re-conceptualize aesthetic vitality as a measurable indicator of systemic physiological resilience. The author describes theoretically proposed organ–skin axes, including the role of molecular signaling of kidney-derived klotho (KL1 fragment) via FGFR1-α–klotho complexes and muscle-derived irisin through the AMPK/PGC-1-α pathway in modulating skin homeostasis. Drawing on recent breakthroughs in non-human primate models (2023–2025), this synthesis explores the potential of systemic interventions—including nicotinamide adenine dinucleotide (NAD+) precursors (sirtuin 1 SIRT1 activators), senolytics (targeting BCL-2/p16), and glucagon-like peptide-1 (GLP-1) receptor agonists—as candidates to potentially synchronize these internal clocks. Furthermore, the review identifies direct regenerative interventions, such as retinoids (RAR/RXR signaling), chemical peels (HIF-1-α induction), exosomes (miR-21/29 delivery), and poly-L-lactic acid PLLA (mechanotransduction via YAP/TAZ), positioning them as potential physical and chemical epigenetic modulators that may support the restoration of cellular transcriptional fidelity. This article proposes a new paradigm for regenerative aesthetics that focuses on restoring the youthful phenotype by optimizing systemic molecular crosstalk and epigenetic transcriptional fidelity. Full article

Maternal stress during lifetime and pregnancy may influence offspring epigenetic age, impacting long-term health. We conducted a systematic review and meta-analysis of associations between maternal stress and epigenetic aging markers: telomere length (TL) and DNA methylation (DNAm) age acceleration. The systematic search was performed according to PRISMA guidelines and registered on PROSPERO (ref. CRD42023474640). Fixed and random effect meta-analyses were carried out, stratified by stress type and marker type (TL, DNAm). Sixteen studies met inclusion criteria; 12 were meta-analyzed (10 TL, 2 DNAm). Due to high heterogeneity, restricted maximum likelihood meta-analysis suggested significant inverse associations between maternal stress and offspring TL. Perceived stress was associated with shorter TL (p-value = 7 × 10⁻⁴, β = −0.085, 95%CI [−0.135, −0.036]), as was lifetime stress/trauma (p-value = 0.01, β = −0.209, 95%CI [−0.370, −0.049]). In contrast, maternal stress showed no significant associations with DNAm age acceleration (p-value = 0.32). Both perceived maternal stress and maternal stress were associated with shorter offspring TL, suggesting that stress exposure across the maternal lifespan influences offspring biological aging markers. No significant association was observed with DNAm-based aging clocks. Further studies with larger sample sizes and more homogeneous settings are needed to confirm and expand upon our observations. Full article

Urban air pollution is increasingly recognised as a determinant of mental wellbeing, yet most existing studies rely on static exposure estimates and lack spatial granularity. This limits understanding of how pollutant-specific patterns influence psychological states in real-world settings. To address this gap, we integrate real-time environmental and physiological data from 40 participants using the DigitalExposome dataset, applying multivariate and spatial analysis techniques. Our findings confirm that Particulate Matter (PM_2.5) exerts the strongest negative association with mental wellbeing while extending prior work by establishing a preliminary ranking of other pollutants Particulate Matter (PM₁₀), Particulate Matter (PM₁), Carbon Monoxide (CO), Nitrogen Dioxide (NO₂), Ammonia (NH₃). We applied statistical and spatial analysis methods, including heatmaps and Voronoi diagrams, to explore links between pollutants and wellbeing and compare the relative influence of air pollution and noise. This enabled identification of pollutant-specific hotspots and multi-level wellbeing patterns across individual, accumulated, and collective scales. These results demonstrate the value of spatial analysis for environmental health research and support targeted urban interventions, such as green space placement and traffic re-routing, to mitigate mental wellbeing risks. Full article