Ethylene Oxide Exposure and Its Impact on Stroke Risk and  All-Cause Mortality: A Population-Based Analysis

Chenxi  Li; Chao  Qi; Yalong  He; Baiya  Fan; Ruyu  Bai

doi:10.18502/ijph.v54i8.19572

Chenxi Li Neurological Department, Yan'an People's Hospital, Yan'an, Shaanxi, 716000, China
Chao Qi Department of Emergency & Critical Care Medicine I, Affiliated Hospital of Shandong, University of Traditional Chinese Medi-cine, Jinan, Shandong, 250000, China
Yalong He Neurological Department, Yan'an People's Hospital, Yan'an, Shaanxi, 716000, China
Baiya Fan Neurological Department, Yan'an People's Hospital, Yan'an, Shaanxi, 716000, China
Ruyu Bai Neurological Department, Yan'an People's Hospital, Yan'an, Shaanxi, 716000, China

DOI: https://doi.org/10.18502/ijph.v54i8.19572

Keywords: Stroke; All-cause mortality; Ethylene oxide

Abstract

Background: Ethylene oxide (EO) is widely used in various industries and has been associated with multiple health risks. However, its impact on stroke risk and all-cause mortality in the general population remains has not been definitively established. This study aimed to investigate the association between EO exposure, stroke risk, and all-cause mortality in a population-based sample.

Methods: Data were obtained from the National Health and Nutrition Examination Survey (NHANES) from 2013 to 2018, involving 29,350 participants. After applying inclusion and exclusion criteria, 4,908 participants with detectable EO levels and complete stroke and mortality data were included in the analysis. Hemoglobin adducts of EO (HbEO) were used as a marker of exposure. Logistic regression models were used to examine the association between EO levels and stroke risk, while Cox proportional hazards models assessed the relationship between EO levels and all-cause mortality, adjusting for covariates such as age, high blood pressure, diabetes, and smoking history.

Results: Higher EO exposure levels were significantly associated with an increased risk of stroke, particularly after adjusting for covariates such as age (OR: 1.002, 95% CI: 1.001-1.003, P<0.0001) and additional covariates (OR: 1.001, 95% CI: 1.000-1.003, P=0.023). Higher EO levels were also associated with increased all-cause mortality when adjusted for age and additional covariates (HR: 1.333, 95% CI: 1.003-1.770, P=0.047).

Conclusion: This study provides evidence of a significant association between EO exposure and increased risks of stroke and all-cause mortality in the general population. Further research is necessary to confirm these findings using direct EO exposure measurements.