Abstract
INTRODUCTION: Population aging is a global concern, with the World Health Organization predicting that by 2030, one in six individuals worldwide will be 60 years or older. Ethylene oxide (EO) is a widely used industrial chemical with potential health risks, including associations with age-related diseases. This study investigates the relationship between EO exposure and biological age acceleration. METHOD: Data from the National Health and Nutrition Examination Survey (NHANES) 2013-2016 were analyzed, including 3,155 participants after exclusions. Blood EO levels were measured using hemoglobin adducts (HbEO). Biological age acceleration was assessed using two methods: Phenotypic Age Acceleration (PhenoAgeAccel) and Klemera-Doubal Method Age Acceleration (KDM-AA). Linear and logistic regression models were applied, adjusting for various covariates, and restricted cubic spline (RCS) regression was used to explore non-linear associations. RESULTS: Higher EO exposure was significantly associated with increased PhenoAgeAccel and KDM-AA across all models. In the continuous model, substantial positive associations were observed (PhenoAgeAccel: β = 0.73, p < 0.001; KDM-AA: β = 0.66, p < 0.001) in Model 3. Quintile analysis indicated a trend of increasing biological age acceleration with higher EO exposure. RCS regression demonstrated a significant linear relationship between EO exposure and PhenoAgeAccel (p for non-linearity = 0.067), as well as with KDM-AA (p for non-linearity = 0.083). Subgroup and interaction analyses revealed significant modifying effects by factors such as body mass index, gender, diabetes status, and physical activity level. CONCLUSION: Our study demonstrates a significant association between EO exposure and accelerated biological aging. These findings highlight the need for further prospective and mechanistic studies to validate and explore this phenomenon.