Environmental Assessment and Evaluation of Oxidative Stress and Genotoxicity Biomarkers Related to Chronic Occupational Exposure to Benzene

Abstract

Environmental and occupational exposure to benzene from fuels is a major cause for concern for national and international authorities, as benzene is a known carcinogen in humans and there is no safe limit for exposure to carcinogens. The objective of this study was to evaluate the genotoxic effects of chronic occupational exposure to benzene among two groups of workers: filling station workers (Group I) and security guards working at vehicles entrances (Group II), both on the same busy highway in Rio de Janeiro, Brazil. Sociodemographic data on the workers were evaluated; the concentration of benzene/toluene (B/T) in atmospheric air and individual trans,trans-muconic acid (ttMA) and S-phenylmercapturic acid (S-PMA) were measured; oxidative stress was analyzed by catalase (CAT), glutathione S-transferase (GST), superoxide dismutase (SOD), thiol groups (THIOL) and malondialdehyde (MDA); genotoxicity was measured by metaphases with chromosomal abnormalities (MCA) and nuclear abnormalities, comet assay using the enzyme formamidopyrimidine DNA glycosylase (C-FPG), and methylation of repetitive element LINE-1, CDKN2B and KLF6 genes. Eighty-six workers participated: 51 from Group I and 35 from Group II. The B/T ratio was similar for both groups, but Group I had greater oscillation of benzene concentrations because of their work activities. No differences in ttMA and S-PMA, and no clinical changes were found between both groups, but linearity was observed between leukocyte count and ttMA; and 15% of workers had leukocyte counts less than 4.5 × 109 cells L−1, demanding close worker’s attention. No differences were observed between the two groups for THIOL, MDA, MCA, or nuclear abnormalities. A multiple linear relationship was obtained for the biomarkers MCA and C-FPG. A significant correlation was found between length of time in current job and the biomarkers C-FPG, MCA, GST, and MDA. Although both populations had chronic exposure to benzene, the filling station workers were exposed to higher concentrations of benzene during their work activities, indicating an increased risk of DNA damage.

Evaluation of some biological parameters of gasoline station attendants in Damascus, Syria

“…Gasoline contains aromatic hydrocarbons like benzene, toluene, ethylbenzene, and xylenes (BTEX), among which benzene has the greatest toxicological risk [ 15 ]. The enzymatic bio-activation of absorbed benzene leads to the formation of ROS, decreases antioxidant activity and hence increases oxidative stress [ 16 ], this leads to damage to the cell components like proteins, lipids and DNA [ 17 ].…”

Clastogenicity and Aneugenicity of 1,4-Benzoquinone in Different Lineages of Mouse Hematopoietic Stem/Progenitor Cells

“…Many previous studies demonstrated that the main target of benzene-induced toxicity is HSPCs [ 19 , 29 , 30 , 31 , 32 ]. Few previous epidemiology studies showed the association between human exposure on benzene and CA such as translocation and aneuploidy [ 3 , 5 , 33 ]. The induction of CA is a potential mechanism underlying benzene-induced leukemogenesis and hematological diseases.…”

Exosomal secretion may be a self‐protective mechanism of its source cells under environmental stress: A study on human bronchial epithelial cells treated with hydroquinone

“…Normal 16HBE cells could be malignantly transformed when treated with HQ and exosomal miR‐221 derived from HQ‐transformed malignant 16HBE cells was associated with the elevated ability of the proliferation of normal recipient cells (Ran Jiang et al, 2020). HQ could regulate the immune response by inhibiting lymphocyte proliferation via blocking DNA synthesis (Costa‐Amaral et al, 2019). HQ could cause DNA strand breaks, DNA‐protein crosslinks, as well as chromosome breaks in HepG2 cells (Luo, Jiang, Geng, Cao, & Zhong, 2008) and sister chromatid exchange in human lymphocytes in vitro (Erexson, Wilmer, & Kligerman, 1985).…”