Endocrine Abstracts

Background: Styrene and ethylbenzene (S/EB), the monomers found in polystyrene (PS) and polyethylene (PE), are known to continuously leach into the environment and food products. The prevalent use of hand sanitizers containing S/EB during the COVID-19 pandemic has heightened concerns about the health implications of S/EB exposure. Notably, the impact of S/EB exposure on the risk of type 2 diabetes mellitus (T2DM) and its interaction with genetic factors in the general population is not well understood. Additionally, the role of oxidative stress in the S/EB-T2DM link warrants further investigation to clarify the biological mechanisms involved.

Methods: In this prospective cohort study of 2219 Chinese adults followed for 6 years, we evaluated the association between S/EB exposure and T2DM incidence. We constructed a Genetic Risk Score (GRS) based on 205 T2DM-related SNPs to assess cumulative genetic effects and examined the interaction between S/EB exposure and GRS using both multiplicative and additive models. We also measured oxidative stress markers (8-hydroxy-2’-deoxyguanosine, 8-iso-prostaglandin F2α, and protein carbonyl) and developed an Oxidative Stress Score (OSS) to explore the potential mediating role of oxidative stress in the S/EB-T2DM association.

Results: A dose-dependent positive correlation was observed between S/EB exposure and T2DM incidence. High levels of S/EB exposure (RR=1.930, 95% CI: 1.157-3.309) and GRS (RR=1.943, 95% CI: 1.110-3.462) were significantly associated with an increased risk of T2DM. Notably, a substantial additive interaction between S/EB exposure and GRS was identified, with a relative excess risk due to interaction of 0.178 (95% CI: 0.065-0.292). Individuals with high S/EB and GRS levels had a markedly elevated risk of T2DM (RR=2.602, 95% CI: 1.238-6.140) compared to those with low levels of both. Oxidative stress was found to partially mediate the relationship between S/EB exposure and T2DM, contributing to 5.98% of the association.

Discussion: This study provides the first clear evidence that S/EB exposure significantly increases the risk of T2DM, with this risk further exacerbated by genetic susceptibility. The role of oxidative stress in this association suggests potential pathways for intervention. These findings could lead to novel strategies for managing S/EB pollution and personalized approaches for T2DM prevention, emphasizing the importance of addressing both environmental and genetic factors in disease risk management.