Trace element exposure and accelerated aging: Epidemiological evidence, biological mechanisms, and public health implications

Background: Trace elements are persistent environmental contaminants that may contribute to biological aging through cumulative effects on molecular, cellular, and physiological processes. Cadmium, lead, mercury, arsenic, and manganese are widely distributed through industrial activity, mining, fossil-fuel combustion, contaminated food and water, agricultural inputs, and occupational settings. Their potential relevance extends beyond recognised organ-specific toxicity because chronic exposure may disrupt pathways associated with aging and age-related disease. Objective: This review synthesised epidemiological and mechanistic evidence on the relationship between trace element exposure, biological aging biomarkers, neurocognitive outcomes, and public-health implications. Methods: A structured narrative review of literature published between 2015 and 2026 was conducted using PubMed and Google Scholar. Search terms covered trace elements, biological aging, epigenetic age acceleration, telomere length, phenotypic age, frailty, cognitive decline, neurodegeneration, and mortality. Eligible evidence included peer-reviewed human observational studies, cohort studies, systematic reviews, meta-analyses, and mechanistic reviews. Twenty-three studies formed the principal evidence synthesis, while additional sources provided methodological, mechanistic, and public-health context. Evidence was interpreted through an exposure-biological embedding-biomarker-clinical outcome-mechanism framework. Results: Cadmium and lead showed the most consistent associations with epigenetic age acceleration, altered telomere biology, phenotypic age acceleration, frailty, cognitive decline, and mortality. Arsenic, mercury, manganese, and mixed-metal exposures were also associated with aging-related biomarkers, although findings varied according to exposure timing, biological matrix, population characteristics, and analytical method. Mechanistic evidence indicated that oxidative stress, mitochondrial dysfunction, epigenetic dysregulation, impaired autophagy, cellular senescence, and chronic inflammation may provide interconnected pathways linking exposure with reduced biological resilience. Cross-sectional designs, single time-point exposure measurements, residual confounding, biomarker variability, and limitations in mixture modelling constrained causal interpretation. Conclusion: Trace elements are credible environmental contributors to biological stress and age-related vulnerability, particularly through chronic cumulative exposure. Current evidence supports precautionary reduction of cadmium and lead exposure, strengthened environmental and occupational monitoring, and protection of vulnerable populations. Longitudinal, life-course, mixture-aware studies incorporating repeated exposure assessment, harmonised aging biomarkers, and clinically meaningful outcomes are needed to clarify causality and guide prevention.