Association between ethylene oxide exposure and prevalence of COPD: Evidence from NHANES 2013–2016

Environmental exposures are major risk factors for chronic obstructive pulmonary disease (COPD). Ethylene oxide (EO) is a ubiquitous organic compound and adversely affects human health. However, it remains unknown whether EO exposure increases the risk of COPD. This study aimed to explore the association between EO exposure and the prevalence of COPD.In this cross-sectional study, 2243 participants were analyzed from the National Health and Nutrition Examination Survey (NHANES) between 2013 and 2016. Participants were classified into four groups according to quartiles of log10-transformed hemoglobin adducts of EO (HbEO) levels. HbEO levels were measured using the modified Edman reaction and high-performance liquid chromatography coupled with tandem mass spectrometry (HPLC-MS/MS). Logistic regression, restricted cubic spline regression model, and subgroup analysis were used to assess whether EO exposure was associated with the risk of COPD. A multivariate linear regression model was used to investigate the correlation between HbEO levels and inflammatory factors. A mediating analysis was conducted to estimate whether inflammatory factors were involved in the effects of HbEO on the prevalence of COPD.Participants with COPD had higher HbEO levels than those without COPD. Log10-transformed HbEO levels were associated with an increased risk of COPD after adjusting for all covariates. [Q4 vs. Q1 in model II: OR = 2.15, 95 % CI: 1.20-3.85, P = 0.010, P for trend = 0.009]. Moreover, a nonlinear J-shaped relationship was observed between HbEO levels and the risk of COPD. Furthermore, HbEO levels were positively correlated with inflammatory cells. In addition, white blood cells and neutrophils mediated the relationship between HbEO and the prevalence of COPD with mediated proportions of 10.37 % and 7.55 %, respectively.These findings indicate that EO exposure has a J-shaped association with the risk of COPD. Inflammation is a key mediator involved in the effects of EO exposure on COPD.