Long-term PM2.5 exposure and type 2 diabetes risk: implications for cardiometabolic health

Abstract Background Type 2 diabetes mellitus (T2DM) is a major contributor to the global cardiometabolic disease burden, associated with increased cardiovascular risk and reduced quality of life. While traditional risk factors like obesity and physical inactivity are well-documented, environmental factors such as air pollution are emerging as critical contributors. Fine particulate matter (PM2.5) exposure, a key component of air pollution, has been implicated in systemic inflammation, oxidative stress, and endothelial dysfunction, all of which play central roles in the development of both T2DM and cardiovascular disease. This study examines the association between long-term PM2.5 exposure and T2DM risk. Purpose The study aimed to investigate the relationship between long-term ambient PM2.5 exposure and the incidence of T2DM. We further sought to highlight the broader implications of air pollution as a modifiable risk factor for cardiometabolic health. Methods A prospective cohort of 16,665 men aged 65-74 years from the VIVA screening trial was analyzed. Participants without pre-existing T2DM at baseline were followed for a mean of 9.3 years. PM2.5 exposure was modeled using the DEHM/UBM/AIRGIS system, which integrates high-resolution geospatial data with emissions and meteorological inputs. Traffic noise exposure, assessed via Nord2000, was included as a potential confounder. Cox proportional hazards models quantified the association between PM2.5 exposure and T2DM risk, adjusting for age, body mass index (BMI), smoking status, socioeconomic factors, and traffic noise. Results During follow-up, 324 participants (1.9%) developed T2DM. Individuals with T2DM had higher mean PM2.5 exposure levels (12.12 µg/m³) compared to non-diabetic participants (11.93 µg/m³; p < 0.001). Each 1.15 µg/m³ increase in long-term PM2.5exposure was associated with a 30.6% higher risk of T2DM (HR: 1.306; 95% CI: 1.08-1.58; p = 0.006). Notably, participants with higher BMI categories exhibited amplified risks, suggesting potential synergistic effects between obesity and air pollution. Conclusion Long-term PM2.5 exposure appears to be significantly associated with an increased risk of T2DM. These findings suggest that air pollution not only impacts respiratory and cardiovascular health but also contributes to metabolic disorders, reinforcing the interconnected nature of cardiometabolic diseases. Public health interventions to reduce PM2.5 exposure, particularly in urban environments, could mitigate the burden of both diabetes and cardiovascular disease. Relevance T2DM is a well-established risk factor for cardiovascular diseases, including myocardial infarction and heart failure. Understanding and addressing environmental contributors such as air pollution is crucial for reducing the overall burden of cardiometabolic disorders. This study highlights the need for interdisciplinary strategies, combining cardiology, public health, and environmental science.