Chen Xinyun, Shi Fangyu, Yu Wenhui, He Chunying, Gou Shenju, Fu Ping
Department of Health Management, Health Management Center, General Practice Center, West China Hospital, Sichuan University, Chengdu, China.
Department of Nephrology, Institute of Kidney Diseases, West China Hospital, Sichuan University, Chengdu, China.
Front Public Health. 2024 Nov 27;12:1488558. doi: 10.3389/fpubh.2024.1488558. eCollection 2024.
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.
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.
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: = 0.73, < 0.001; KDM-AA: = 0.66, < 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 ( for non-linearity = 0.067), as well as with KDM-AA ( 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.
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.
人口老龄化是一个全球关注的问题，世界卫生组织预测，到2030年，全球每六个人中就有一个年龄在60岁及以上。环氧乙烷（EO）是一种广泛使用的工业化学品，具有潜在的健康风险，包括与年龄相关疾病的关联。本研究调查了环氧乙烷暴露与生物年龄加速之间的关系。
分析了2013 - 2016年国家健康与营养检查调查（NHANES）的数据，排除后包括3155名参与者。使用血红蛋白加合物（HbEO）测量血液中的环氧乙烷水平。使用两种方法评估生物年龄加速：表型年龄加速（PhenoAgeAccel）和克莱梅拉 - 杜巴尔方法年龄加速（KDM - AA）。应用线性和逻辑回归模型，并对各种协变量进行调整，使用受限立方样条（RCS）回归来探索非线性关联。
在所有模型中，较高的环氧乙烷暴露与PhenoAgeAccel和KDM - AA的增加显著相关。在连续模型中，模型3中观察到显著的正相关（PhenoAgeAccel：β = 0.73，P < 0.001；KDM - AA：β = 0.66，P < 0.001）。五分位数分析表明，随着环氧乙烷暴露增加，生物年龄加速呈上升趋势。RCS回归表明环氧乙烷暴露与PhenoAgeAccel之间存在显著的线性关系（非线性检验P = 0.067）以及与KDM - AA之间也存在显著线性关系（非线性检验P = 0.083）。亚组和交互分析揭示了体重指数、性别、糖尿病状态和身体活动水平等因素的显著调节作用。
我们的研究表明环氧乙烷暴露与生物衰老加速之间存在显著关联。这些发现突出了进一步进行前瞻性和机制性研究以验证和探索这一现象的必要性。
