PubMed | c Henan Provincial Institute of Occupational Health, Texas Tech University and National Institute for Occupational Health and Poison Control
Type: Journal Article | Journal: Free radical research | Year: 2016
Diesel engine exhaust (DEE) was found to induce lipid peroxidation (LPO) in animal exposure studies. LPO is a class of oxidative stress and can be reflected by detecting the levels of its production, such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), and etheno-DNA adducts including 1,N(6)-etheno-2-deoxyadenosine (dA) and 3,N(4)-etheno-2-deoxycytidine (dC). However, the impact of DEE exposure on LPO has not been explored in humans. In this study, we evaluated urinary MDA, 4-HNE, dA, and dC levels as biomarkers of LPO among 108 workers with exclusive exposure to DEE and 109 non-DEE-exposed workers. Results showed that increased levels of urinary MDA and dA were observed in subjects occupationally exposed to DEE before and after age, body mass index (BMI), smoking status, and alcohol use were adjusted (all p<0.001). There was a statistically significant relationship between the internal exposure dose (urinary OH-PAHs) and MDA, 4-HNE, and dA (all p<0.001). Furthermore, significant increased relations between urinary etheno-DNA adduct and MDA, 4-HNE were observed (all p<0.05). The findings of this study suggested that the level of LPO products (MDA and dA) was increased in DEE-exposed workers, and urinary MDA and dA might be feasible biomarkers for DEE exposure. LPO induced DNA damage might be involved and further motivated the genomic instability could be one of the pathogeneses of cancer induced by DEE-exposure. However, additional investigations should be performed to understand these observations.