Type 1 diabetes (T1D) is a complex autoimmune disorder characterized by the selective destruction of insulin-producing pancreatic β-cells. While genetic predisposition establishes susceptibility, environmental factors play a pivotal role in triggering and modulating the autoimmune process. This narrative review synthesizes current evidence from epidemiological, clinical, and experimental studies to elucidate the mechanisms by which environmental exposures influence the pathogenesis and progression of T1D. We discuss how persistent organic pollutants, heavy metals, air pollutants, viral infections, and gut microbiome alterations contribute to β-cell dysfunction, loss of immune tolerance, and enhanced autoimmunity. Our analysis reveals that these environmental triggers act through multiple interconnected pathways, including oxidative stress, mitochondrial dysfunction, epigenetic modifications, innate immune activation, and gut barrier disruption. Understanding these mechanisms provides critical insights for developing preventive strategies and targeted interventions to mitigate environmental risks. These findings underscore the importance of addressing environmental exposures as modifiable risk factors, offering a potential framework for early interventions aimed at preventing or slowing T1D progression in at-risk populations.
Tang et al. (Sun,) studied this question.