Insulin resistance and its relationship with long-term exposure to ozone: Data based on a national population cohort

The relationship of ozone (O3), particularly the long-term exposure, with impacting metabolic homeostasis in population was understudied and under-recognised. Here, we used data from ChinaHEART, a nationwide, population-based cohort study, combined with O3 and PM2.5 concentration data with high spatiotemporal resolution, to explore the independent association of exposure to O3 with the prevalence of insulin resistance (IR). Among the 271 540 participants included, the crude prevalence of IR was 39.1%, while the age and sex standardized prevalence stood at 33.0%. Higher IR prevalence was observed with each increase of 10.0 μg/m3 in long-term O3 exposure, yielding adjusted odds ratios (OR) of 1.084 (95% CI: 1.079−1.089) in the one-pollutant model and 1.073 (95% CI: 1.067−1.079) in the two-pollutant model. Notably, a significant additive interaction between O3 and PM2.5 on the prevalence of IR was observed (P for additive interaction < 0.001). Our main findings remained consistent and robust in the sensitivity analyses. Our study suggests long-term exposure to O3 was independently and positively associated with prevalence of IR. It emphasized the benefits of policy interventions to reduce O3 and PM2.5 exposure jointly, which could ultimately alleviate the health and economic burden related to DM. Ambient ozone pollution has posed greater challenges to environmental security and public health worldwide; however, little is known about the associations of ambient ozone exposure with insulin resistance (IR), steadily increasing worldwide and leading to a substantial economic and healthcare burden. In this study of more than 0.25 million Chinese community-based participants, we observed a positive association between ozone exposure and IR, especially among specific population. Notably, we found a synergistic interaction between ozone and fine particulate matter on IR. It is noteworthy that implementing targeted policies and interventions may protect these vulnerable populations from pollutants-induced metabolic damage.