Prenatal exposure to environmental toxicants and their association with alterations in kidney development.

HEAVY METAL TOXICITY AND CHRONIC KIDNEY DISEASE IN SOUTHERN TAMIL NADU: CHALLENGES, MECHANISMS, AND PUBLIC HEALTH PERSPECTIVES

Chronic Kidney Disease (CKD) represents a significant global health burden, characterized by a progressive decline in renal function. While traditional risk factors such as diabetes and hypertension are well-established, the role of environmental pollutants, particularly heavy metals, in the etiology and progression of CKD is gaining increasing attention. This comprehensive review synthesizes current knowledge on the impact of heavy metal exposure on CKD, with a specific focus on findings from the Southern Tamil Nadu population. It delvesinto the mechanisms by which various heavy metals, including but not limited to arsenic, lead, cadmium, and mercury, exert nephrotoxic effects, leading to cellular damage, glomerulosclerosis, and impaired renal function. The review also examines the prevalence of heavy metal exposure in susceptible populations, routes of exposure, and the challenges in establishing clear causal links due to the heterogeneity of environmental factors and population demographics. Furthermore, it discusses diagnostic approaches, potential therapeutic interventions, and the critical need for effective management strategies to mitigate the adverse health outcomes associated with heavy metal-induced nephropathy. By integrating findings from recent studies and highlighting the uniquecontext of Southern Tamil Nadu, this review aims to provide a deeper understanding of this complex public health issue and underscore the importance of environmental monitoring and public health interventions to prevent and manage CKD.

LITERATURE REVIEW Early-life environmental exposures and pediatric cardiovascular health

Urban Environmental Exposures, Air Pollution, and Maternal–Offspring Outcomes: A Systematic Review

Background: Urban ambient air pollution and various co-occurring environmental stressors during pregnancy contribute to systemic inflammation, oxidative stress, endothelial dysfunction, and impaired placental perfusion, thereby increasing the risk of adverse maternal and child health outcomes. Therefore, this study aims to systematically synthesize the evidence on the associations between ambient air pollution and co-occurring urban environmental exposures and pregnancy complications affecting maternal and child health, based on the available evidence.Methods: Following PRISMA 2020 guidelines and a defined PECO framework, comprehensive searches were executed on Scopus and ScienceDirect (April 23, 2026; updated May 06, 2026) for literature published between 2022 and 2025. Of 3,547 records identified, 20 articles met the inclusion criteria, comprising 16 empirical observational studies and 4 supporting conceptual articles. Study quality and risk of bias were assessed using the Newcastle-Ottawa Scale and JBI critical appraisal tools.Results: Moderate-certainty evidence indicated that exposure to PM2.5 and NO2 during the preconception and early-to-mid pregnancy periods increased the risks of gestational diabetes mellitus, hypertensive disorders of pregnancy, low birth weight, and preterm birth. Multi-pollutant models consistently provided stronger risk estimates than single-pollutant models. Evidence linking air pollution with gestational hypothyroidism, postpartum mental distress, and offspring neurodevelopmental outcomes remained limited and heterogeneous.Conclusion: Ambient air pollution and related urban environmental exposures are important determinants of maternal and child health. Integrating environmental exposure assessment into antenatal care and strengthening urban emission reduction policies are essential to reduce pregnancy-related health risks.

Environmental Pollution Exposure and Its Impact on Mental and Reproductive Health: A Review

Environmental pollution is a growing global public health threat and is not limited to classic cardiopulmonary effects, impeding numerous physiological systems. Evidence of an association between environmental contaminant exposures and poor mental health, neurodevelopmental, reproductive, and pregnancy outcomes is increasing. The current evidence on main pollution sources, such as atmospheric pollution, endocrine-disrupting chemicals, heavy metals, persistent organic pollutants, pesticides, per- and polyfluorocarbons (PFAS), and emerging contaminants such as microplastics, is summarized, along with underlying biological mechanisms and public health implications. A narrative review was conducted of peer-reviewed literature, and linkages between environmental exposures and mental, reproductive, and pregnancy-related outcomes were addressed. Studies on air pollutants, bisphenols, phthalates, lead, mercury, and cadmium, pesticides, PFAS, polychlorinated biphenyls, dioxins, and microplastics were all included. The focus was on pinpointing common mechanistic features and merging together results with the exposome approach that considers exposure to the environment throughout an individual’s life. When cells are continually exposed to various environmental pollutants, there is increasing evidence of these substances being linked to depression, anxiety, cognitive dysfunction, abnormalities in neurodevelopment, worsening semen quality, diminished fecundability, ovarian dysfunction, abnormalities in sexual maturation, and harmful pregnancy effects such as damage to the placenta or developmental defects in the fetus. These effects involve interrelated pathways including oxidative stress, neuroinflammation, endocrine disruption, mitochondrial dysfunction, immune dysregulation, vascular injury, and epigenetic changes. Further, it is possible that exposure to a combination of pollutants may result in additive or synergistic effects, leading to effects that are greater than would be caused by any individual pollutant, increasing vulnerability in sensitive groups such as pregnant women, infants, children, and socioeconomically disadvantaged groups. The exposome allows us to frame these exposures in a comprehensive way to understand these cumulative and lifelong exposures. The issue of environmental pollution severely affects mental and reproductive health and is an increasing health threat. The current evidence suggests that there is an urgent need to reinforce regulatory policies, exposure monitoring, and a surge in surveillance of health effects. Future studies should focus on longitudinal exposures, mixture exposure indicators, and using data on the exposome to understand risk and to find vulnerable human groups. There is a strong need to strengthen environmental health policies, particularly to mitigate and prevent disease burden and ensure population health in an environment with an ever-increasing disease burden and negative impacts of pollution.

Developmental origins of hypertension and renal injury: epigenetic memory in renal stem and progenitor cells.

Nicotine Exposure During Gestation: From Placental Dysfunction to Long-Term Neurobehavioral Outcomes.

BACKGROUND Prenatal nicotine exposure (PNE) remains a significant public health concern due to persistent tobacco use, electronic nicotine delivery systems, and second-hand exposure during pregnancy. Epidemiological and experimental evidence has demonstrated that nicotine can readily cross the placenta, disrupt placental development, and interfere with tightly regulated processes of fetal organogenesis. These early perturbations are increasingly recognized as initiating a cascade of structural, functional, and molecular alterations that extend beyond gestation and influence health trajectories across the lifespan. However, existing studies are often compartmentalized by developmental stage, limiting mechanistic integration across prenatal, natal, postnatal, and later-life outcomes. METHODS This review aims to (i) synthesize evidence from placental biology, developmental toxicology, neurobiology, and epigenetics to propose an integrated, life-course cascade model of PNE; (ii) delineate how nicotine-induced placental dysfunction and fetal hypoxia during prenatal development transition into structural, physiological, perinatal autonomic, and cardiorespiratory vulnerability, contributing to adverse birth outcomes and increased risk of sudden infant death syndrome; and (iii) examine how early disruption of nicotinic acetylcholine receptor mediated signaling alters neuronal differentiation, synaptic maturation, neuroimmune interactions, and stress-response pathways, leading to persistent cognitive, behavioral, and psychiatric susceptibility in postnatal life and adulthood. Emerging evidence for epigenetic reprogramming, sex-specific vulnerability, and intergenerational transmission, including paternal contributions, is also evaluated. RESULTS Evidence synthesized across placental biology, developmental toxicology, neurobiology, and epigenetics supports a cascade in which nicotine-induced placental dysfunction and fetal hypoxia contribute to structural, physiological, perinatal autonomic, and cardiorespiratory vulnerability, adverse birth outcomes, and increased risk of sudden infant death syndrome. Early disruption of nicotinic acetylcholine receptor-mediated signaling is associated with alterations in neuronal differentiation, synaptic maturation, neuroimmune interactions, and stress-response pathways, contributing to persistent cognitive, behavioral, and psychiatric susceptibility in postnatal life and adulthood. Emerging evidence also supports roles for epigenetic reprogramming, sex-specific vulnerability, and intergenerational transmission, including paternal contributions. CONCLUSION By integrating temporally distinct findings into a unified mechanistic framework, this review identifies critical developmental windows and molecular targets for intervention. Such an approach is essential for advancing preventive strategies, informing public health policy, and mitigating the long-term and transgenerational consequences of nicotine exposure.