Benzene Induces Cytotoxicity without Metabolic Activation

Nishikawa, Takuro; Izumo, Kimiko; Miyahara, Emiko; Horiuchi, Masahisa; Okamoto, Yasuhiro; Kawano, Yoshifumi; Takeuchi, Tōru

doi:10.1539/joh.10-002-oa

Cited by 16 publications

(13 citation statements)

References 37 publications

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“…The results suggest that benzene‐associated DNA damage was probably due to nucleic acid oxidation by oxidative stress. This is supported by the reports that showed that benzene metabolites exert their toxicity via production of ROS (Uzma et al ., ; Nishikawa et al ., ) and cumulative benzene exposure causes oxidation of nucleic acid (Manini et al ., ) and other biological macromolecules (Bagryantseva et al ., ). Besides benzene, particulate matters, especially ultrafine particles which are abundant in biomass smoke, can produce ROS directly because of the presence of free radicals and oxidants adsorbed on their surface (Fubini et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene

Mukherjee

Dutta

Roychoudhury

et al. 2011

J of Applied Toxicology

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This study examined whether indoor air pollution from biomass fuel burning induces DNA damage in airway cells. For this, sputum cells were collected from 56 premenopausal rural women who cooked with biomass (wood, dung, crop residues) and 49 age-matched controls who cooked with cleaner liquefied petroleum gas. The levels of particulate matters with diameters of less than 10 and 2.5 µm (PM(10) and PM(2.5)) in indoor air were measured using a real-time aerosol monitor. Benzene exposure was monitored by measuring trans,trans-muconic acid (t,t-MA) in urine by HPLC-UV. DNA damage was examined by alkaline comet assay in sputum cells. Generation of reactive oxygen species (ROS) and level of superoxide dismutase (SOD) in sputum cells were measured by flow cytometry and spectrophotometry, respectively. Compared with controls, biomass users had 4 times higher tail percentage DNA, 37% more comet tail length and 5 times more Olive tail moment (p < 0.001) in inflammatory and epithelial cells in sputum, suggesting extensive DNA damage. In addition, women who cooked with biomass had 6 times higher levels of urinary t,t-MA and 2-fold higher levels of ROS generation concomitant with 28% depletion of SOD. Indoor air of biomass-using households had 2-4 times more PM(10) and PM(2.5) than that of controls. After controlling potential confounders, positive association was found between DNA damage parameters, particulate pollution, urinary t,t-MA and ROS. Thus, long-term exposure to biomass smoke induces DNA damage in airway cells and the effect was probably mediated, at least in part, by oxidative stress generated by inhaled particulate matter and benzene.

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Section: Discussionmentioning

confidence: 99%

Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene

Mukherjee

Dutta

Roychoudhury

et al. 2011

J of Applied Toxicology

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“…However, no significant global DNA methylation changes were observed in a study using normal hepatic L02 cells or human myeloid HL-60 cells that were incubated with benzene for 48 hours and which displayed changes in gene expression levels [113, 114], although the exposure concentrations tested were similar or higher than those used in the Tabish et al [112] study.…”

Section: Epigenetic Effects Associated With Carcinogenic Chemicalsmentioning

confidence: 99%

Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review

Chappell

Pogribny

Guyton

et al. 2016

Mutation Research/Reviews in Mutation Research

142

105

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Accumulating evidence suggests that epigenetic alterations play an important role in chemically-induced carcinogenesis. Although the epigenome and genome may be equally important in carcinogenicity, the genotoxicity of chemical agents and exposure-related transcriptomic responses have been more thoroughly studied and characterized. To better understand the evidence for epigenetic alterations of human carcinogens, and the potential association with genotoxic endpoints, we conducted a systematic review of published studies of genotoxic carcinogens that reported epigenetic endpoints. Specifically, we searched for publications reporting epigenetic effects for the 28 agents and occupations included in Monograph Volume 100F of the International Agency for the Research on Cancer (IARC) that were classified as “carcinogenic to humans” (Group 1) with strong evidence of genotoxic mechanisms of carcinogenesis. We identified a total of 158 studies that evaluated epigenetic alterations for 12 of these 28 carcinogenic agents and occupations (1,3-butadiene, 4-aminobiphenyl, aflatoxins, benzene, benzidine, benzo[a]pyrene, coke production, formaldehyde, occupational exposure as a painter, sulfur mustard, and vinyl chloride). Aberrant DNA methylation was most commonly studied, followed by altered expression of non-coding RNAs and histone changes (totaling 85, 59 and 25 studies, respectively). For 3 carcinogens (aflatoxins, benzene and benzo[a]pyrene), 10 or more studies reported epigenetic effects. However, epigenetic studies were sparse for the remaining 9 carcinogens; for 4 agents, only 1 or 2 published reports were identified. While further research is needed to better identify carcinogenesis-associated epigenetic perturbations for many potential carcinogens, published reports on specific epigenetic endpoints can be systematically identified and increasingly incorporated in cancer hazard assessments.

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“…Therefore, human exposure to benzene is of particular concern because epidemiologic studies, [5][6][7][8] recommendations from public and federal health agencies, 9,10 and consensus statements from medical organizations 11 suggest that it can result in chronic toxicity, with an increased risk of carcinogenesis. [12][13][14][15] The hematologic toxicity of benzene poisoning has been well documented in the literature. 3,15,16 It is well established that benzene exposure can induce blood disorders leading to hematopoietic malignancies and other cancers.…”

Section: In Nt Tr Ro Od Du Uc Ct Ti Io On Nmentioning

confidence: 99%

Health consequences of involuntary exposure to benzene following a flaring incident at British Petroleum refinery in Texas City

D’Andrea¹,

Singh²,

Reddy³

2013

Am J Disaster Med

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Benzene Induces Cytotoxicity without Metabolic Activation

Abstract: Benzene Induces Cytotoxicity without Metabolic Activation: Takuro Nishikawa, et al.

Cited by 16 publications

References 37 publications

Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene

Chronic inhalation of biomass smoke is associated with DNA damage in airway cells: involvement of particulate pollutants and benzene

Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review

Health consequences of involuntary exposure to benzene following a flaring incident at British Petroleum refinery in Texas City

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