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Microplastics, endocrine-disrupting chemicals, persistent environmental pollutants, oxidative stress, non-communicable diseases, particulate matter, heavy metals
Summary
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.
Research objective: Environmental exposure to endocrine-disrupting chemicals (EDCs), micro- and nanoplastics (MNPs), particulate matter (PM2.5), heavy metals, and pesticides represents an increasing global health concern. This review aimed to summarize the major mechanisms underlying their toxicity and their links to human disease. Methodology: A narrative review of experimental and epidemiological literature was conducted to synthesize current evidence on the toxicity mechanisms and health effects of environmental pollutants. Main conclusions: The major mechanisms underlying pollutant toxicity include oxidative stress, chronic inflammation, endocrine disruption, epigenetic modification, and genotoxicity. These processes have been linked to reproductive dysfunction, neurodegeneration, cardiovascular disease, immune dysregulation, and carcinogenesis. EDCs interfere with hormonal signaling, while MNPs can cross biological barriers and act as carriers for toxic co-contaminants such as heavy metals and persistent organic pollutants. Experimental and epidemiological evidence suggests that chronic exposure may impair fertility, disrupt fetal development, promote systemic inflammation, and contribute to cancer-related pathways. Additional pollutants, including PM2.5 and pesticides, further exacerbate oxidative stress, endothelial dysfunction, and gut microbiome imbalance. Although mechanistic evidence is substantial, human studies remain limited by methodological variability and insufficient longitudinal data. Application of the study: The findings may support clinicians, researchers, and policymakers in recognizing the contribution of environmental pollutants to the burden of non-communicable diseases, informing preventive measures and stronger regulatory strategies. Originality/Novelty of the study: This review integrates mechanistic and epidemiological evidence across multiple classes of environmental pollutants, highlighting their shared toxicity pathways and combined contribution to non-communicable disease risk, while identifying key methodological gaps that warrant further research.