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Molecular Mechanisms of Environmental Pollutants in Human Health for Unravelling the Pathophysiology of Chronic Diseases
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This review examined the integrated molecular mechanisms by which environmental pollutants—including heavy metals, persistent organic pollutants, endocrine disruptors, and microplastics—contribute to chronic diseases such as cancer, cardiovascular disease, and neurodegenerative conditions. The authors found that multiple pollutant classes converge on oxidative stress, epigenetic modification, and inflammatory signaling as shared pathogenic pathways.
Environmental pollutants, including heavy metals, persistent organic pollutants (POPs), endocrine-disrupting chemicals (EDCs), particulate matter, and emerging contaminants such as microplastics, are increasingly associated with the development of chronic human diseases. While the toxicological effects of individual pollutant classes are well established, the integrated molecular mechanisms that link chronic exposure to long-term pathological outcomes remain poorly defined. It is a systematic, mechanistic-oriented review that summarizes the results of 214 epidemiological, experimental, and multi-omics studies to form a concise model of biological disturbance caused by contaminants. The information retrieved in PubMed, Scopus, Web of Science, and ScienceDirect was reviewed, considering the pollutant-targeted modification of oxidative stress, inflammatory signaling, mitochondrial dysfunction, genomic instability, and epigenetic reprogramming. The highest oxidative signature was observed with heavy metals, where 84.1% of the studies indicated redox imbalance, and particulate matter stimulated the greatest inflammatory response (88.5%). POPs exhibited strong epigenetic (71.2%) effects, and EDCs had serious impacts on hormonal and gene-regulatory pathways. Quantitative synthesis revealed a 42.6% rise in reactive oxygen species, a 92.6% increase in lipid peroxidation, and a 28–32% reduction in key antioxidant enzymes and ATP production among exposed populations. Mitochondrial membrane potential declined by 27.8%, and epigenetic markers, including DNA methylation profiles and microRNA expression, showed persistent dysregulation with evidence of transgenerational retention. Multi-omics integration revealed a 71% convergence across disrupted pathways, identifying mitochondrial impairment, NF-κB–mediated inflammation, DNA repair inhibition, and epigenetic remodeling as central mechanistic hubs. The integrated model developed through this review provides a comprehensive explanation of how pollutant exposure increases the risk of cardiometabolic, respiratory, neurodegenerative, and metabolic diseases. These findings underscore the need for biomarker-based risk assessment, mixture-toxicity research, and longitudinal multi-omics studies to enhance disease prediction and prevention.
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Microplastics, endocrine-disrupting chemicals, persistent environmental pollutants, oxidative stress, non-communicable diseases, particulate matter, heavy metals
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Everyday exposures—microplastics, chemicals that mess with your hormones, air pollution, heavy metals, and pesticides—may team up in your body to cause cell damage and inflammation linked to fertility problems, heart disease, developmental issues, and cancer. This review pulls together existing research to show these pollutants often share the same harmful pathways, which helps explain why chronic exposure adds up over time. While more long-term human studies are needed, the evidence is strong enough to matter for how we think about prevention and pollution regulations.
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This review examines how environmental pollutants, including microplastics, heavy metals, and endocrine-disrupting chemicals, can alter immune function through epigenetic changes that modify gene expression without changing DNA itself. Researchers identified common molecular pathways through which these pollutants trigger inflammation and immune disruption. The study also highlights evidence that some of these epigenetic changes may be passed to future generations.
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Researchers synthesized 2020–2025 evidence on how environmental pollutants including micro- and nanoplastics amplify reactive oxygen species through shared nodes — mitochondrial disruption, NADPH oxidase activation, and Fenton chemistry — propagating oxidative signals into epigenetic remodeling, while comparing biomarker platforms by analytical specificity and translational readiness.
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