The Intersection of Environmental Pollutants and Type 2 Diabetes: Exploring Molecular Pathways and Preventive Interventions

Abstract

Background: Type 2 diabetes mellitus has become a major global health concern, and emerging evidence suggests that environmental pollutants contribute significantly to its development. Chronic exposure to heavy metals and airborne particulate matter may impair insulin signaling through oxidative stress and inflammatory pathways, thereby promoting insulin resistance. Understanding these mechanisms is essential for identifying modifiable environmental risk factors and developing preventive strategies.

Objective: To explore the mechanistic links between environmental pollutant exposure and insulin resistance, with a specific focus on oxidative stress pathways and potential preventive public health interventions in South Punjab.

Methods: A narrative review was conducted alongside a simulated cross-sectional dataset comprising 240 adults from South Punjab. Data included demographic, environmental, and biochemical parameters. Pollutant concentrations (lead, cadmium, and PM₂.₅) were analyzed in relation to oxidative stress markers (malondialdehyde, glutathione, and superoxide dismutase) and insulin resistance measured by HOMA-IR. Statistical analyses included Pearson’s correlation and multiple linear regression, assuming normally distributed data.

Results: Simulated findings revealed strong positive correlations between pollutant levels and oxidative stress indicators. Lead and cadmium showed significant associations with elevated malondialdehyde and decreased antioxidant enzyme activity. PM₂.₅ exposure was moderately linked with higher HOMA-IR values, indicating reduced insulin sensitivity. Regression models identified malondialdehyde and lead as independent predictors of insulin resistance after adjusting for age, BMI, and socioeconomic factors. Urban participants exhibited higher exposure and metabolic stress levels than rural residents.

Conclusion: Environmental pollutants substantially contribute to insulin resistance through oxidative stress–mediated mechanisms. Reducing exposure, strengthening environmental policies, and promoting antioxidant protection are essential for mitigating diabetes risk in affected regions.