Exposure–Adaptive Capacity Framework for Environmental Chemical Mixtures and Metabolic Resilience: A Critical Review and Operational Proposal

From molecular responses to environmental monitoring: advances and translational gaps in omics approaches in fish environmental toxicology

Environmental Genotoxins and Human Health Risks: Exposure Pathways, Mechanisms, Biomarkers and Challenges for Causal Risk Assessment

This critical narrative review integrates evidence on major environmental genotoxin classes, exposure routes, molecular mechanisms, human biomonitoring, disease associations and risk-assessment practice for well-established and less mature evidence domains.

Nanoplastics as potential environmental amplifiers of metabolic vulnerability: A systems perspective.

Nanoplastics (NPs) are increasingly recognised as ubiquitous environmental pollutants, and evidence continues to mount that humans are exposed to NPs primarily through food and drinking water. Whilst their presence in biological systems is well documented, their role in metabolic dysfunction remains unclear. Metabolic disorders such as obesity, insulin resistance and non-alcoholic fatty liver disease are characterised by chronic inflammation, impaired energy metabolism and endocrine disruption; under these conditions, the metabolic system itself is subjected to a state of persistent stress. Existing evidence suggests that NPs may directly induce metabolic disorders. However, their impact on metabolism appears to depend heavily on host susceptibility. We therefore propose, as a working hypothesis, the 'metabolic vulnerability amplification model', which posits that NPs do not act merely as independent metabolic toxins, but may amplify pre-existing metabolic stress. In this review, we integrated evidence at the molecular, cellular and organ levels, focusing on mitochondrial dysfunction, chronic inflammation and endocrine disruption, to examine metabolic abnormalities caused by NPs at a systems level. Furthermore, we summarise emerging mitigation strategies, highlight key knowledge gaps relating to chronic low-dose exposure and in vivo dose profiling, and outline priorities for future research. Overall, this study suggests that, under specific conditions of exposure and host susceptibility, NPs may compromise metabolic resilience.

Climate Change as a Determinant of Mental and Physical Health: A Review

Environmental pollution is now a leading public health crisis around the world and fulfills the criteria of an environmental risk factor that impacts more than the well-recognized cardiopulmonary diseases; it is now recognized to affect mental, neurodevelopmental, reproductive, and pregnancy health as well. The goal of this review was to consolidate existing evidence on the effects of environmental pollutants, including air pollutants, endocrine-disrupting chemicals, heavy metals, persistent organic pollutants, pesticides, per- and polyfluoroalkyl substances (PFAS) and emerging pollutants such as microplastics, and the shared biological processes that connect these exposures to harmful health effects. A narrative review of all peer-reviewed publications from 2000 to 2025 was performed by searching through PubMed/MEDLINE, Scopus and Web of Science. Studies examining associations of environmental pollutants and mental health, neurodevelopmental, reproductive, and pregnancy outcomes were reviewed with a focus on systematic reviews, meta-analyses, cohort studies, biomonitoring investigations, and mechanistic studies. Cumulative and lifelong environmental exposures were assessed by evidence synthesis based on the exposome framework. The studied evidence shows consistent relationships between PM, NO 2 , bisphenols, phthalates, PFAS, pesticides, heavy metals (specifically lead, mercury, and cadmium), polychlorinated biphenyls, dioxins and microplastics and elevated risk of depression, anxiety, cognitive impairment, impaired neurodevelopment, decreased semen quality, diminished fecundability, ovarian dysfunction, altered pubertal development, adverse pregnancy outcomes, placental injury, and fetal growth abnormalities. These harmful effects are achieved via common biological pathways such as oxidative stress, neuroinflammation, endocrine disruption, mitochondrial dysfunction, immune dysregulation, vascular injury, and epigenetic changes. There is also evidence that combined exposure to several pollutants can have additive or synergistic effects, and that sensitive groups to pollution exposure include pregnant women, children, and socio-economically disadvantaged groups. Pollution has emerged as an important and increasing concern from a life course perspective on mental and reproductive health. The exposome concept provides a simplified framework to understand cumulative environmental exposures and their health effects. Enforcing polluter accountability, curbing the use of hazardous substances, better monitoring exposure to pollution, better monitoring of reproductive and mental health outcomes, and incorporating pollution into public health policies are critical steps to curbing the disease burden of pollution and to safeguarding sensitive populations.

Human Health Effects of Chronic Microcystin Exposure: A Systematic Review and Meta-Analysis of Hepatic, Renal, and Metabolic Outcomes

Microcystins (MCs) are cyanobacterial hepatotoxins that contaminate bloom-affected freshwater, drinking-water sources, aquatic food webs, and recreational environments. Human evidence for chronic or repeated exposure remains fragmented across study designs and organ systems. We systematically reviewed epidemiological evidence for hepatic, renal, and metabolic outcomes and integrated supporting mechanistic toxicology. PubMed, Scopus, and Web of Science searches identified 9021 records published from 1990 to 2025; an update search was conducted in April 2026. Risk of bias was assessed using a domain-based framework adapted from the Newcastle–Ottawa Scale and OHAT. The review was not prospectively registered. The qualitative evidence architecture retained 192 studies: 34 human epidemiological studies and 158 supporting mechanistic or contextual studies. Only seven independent adjusted estimates met the one-study–one-main-estimate rule for the primary quantitative synthesis. The hepatic meta-analysis included two estimates (OR 2.13; 95% CI, 1.29–3.53), the renal finding was a descriptive single-study estimate (OR 4.81; 95% CI, 1.96–11.81), and the metabolic meta-analysis included four estimates (OR 1.73; 95% CI, 1.00–2.98) with substantial heterogeneity (I2 = 91%; prediction interval, 0.56–5.36). Mechanistic evidence supported biological plausibility but was not treated as causal human evidence. Human evidence was relatively more consistent for hepatic outcomes, although it remained limited to two independent studies with different endpoints; renal and metabolic findings remain sparse or heterogeneous.

The Environmental Contribution to Health and Disease: Analytical Tools for Monitoring and Diagnosis

Environmental exposures throughout life play a major role in shaping human health and contribute to the onset and progression of numerous chronic diseases, including neurodegenerative disorders and cancer. These effects arise from complex interactions between environmental pollutants, diet, lifestyle, occupation, genetic background, and other biological and socioeconomic factors. Although recent advances in omics technologies have substantially improved our understanding of the molecular mechanisms underlying these interactions, most studies continue to adopt reductionist approaches that fail to capture the complexity of the environment–health–disease continuum. We propose a comprehensive conceptual framework based derived from the existing literature for investigating lifelong environmental exposures through a multilevel and multidimensional strategy. Four complementary levels are defined: (i) molecular alterations characterized using ionomics, metallomics, proteomics, metabolomics, transcriptomics, genomics, and integrated multi-omics; (ii) tissue and organ alterations assessed by imaging technologies and radiomics; (iii) population-level variability investigated through epidemiological approaches (epidemiomics); and (iv) the integration and interpretation of heterogeneous datasets using artificial intelligence. Representative applications of these methodologies are discussed to illustrate their potential for identifying biomarkers, elucidating disease mechanisms, and improving exposure assessment. Particular attention is given to the integration of molecular, imaging, and epidemiological data to establish more robust causal relationships between environmental exposures and health outcomes. The proposed framework highlights the need for multidisciplinary collaboration and advanced computational tools to address the complexity of exposome research. Ultimately, this integrative approach may support early disease detection, personalized prevention strategies, and the development of evidence-based environmental, occupational, and public health policies aimed at reducing the burden of environment-related diseases.